Journal articles: 'Enzymes; Breast cancer'

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Wright, Roni H. G., and Miguel Beato. "Role of the NUDT Enzymes in Breast Cancer." International Journal of Molecular Sciences 22, no. 5 (February 25, 2021): 2267. http://dx.doi.org/10.3390/ijms22052267.

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Despite global research efforts, breast cancer remains the leading cause of cancer death in women worldwide. The majority of these deaths are due to metastasis occurring years after the initial treatment of the primary tumor and occurs at a higher frequency in hormone receptor-positive (Estrogen and Progesterone; HR+) breast cancers. We have previously described the role of NUDT5 (Nudix-linked to moiety X-5) in HR+ breast cancer progression, specifically with regards to the growth of breast cancer stem cells (BCSCs). BCSCs are known to be the initiators of epithelial-to-mesenchyme transition (EMT), metastatic colonization, and growth. Therefore, a greater understanding of the proteins and signaling pathways involved in the metastatic process may open the door for therapeutic opportunities. In this review, we discuss the role of NUDT5 and other members of the NUDT family of enzymes in breast and other cancer types. We highlight the use of global omics data based on our recent phosphoproteomic analysis of progestin signaling pathways in breast cancer cells and how this experimental approach provides insight into novel crosstalk mechanisms for stratification and drug discovery projects aiming to treat patients with aggressive cancer.

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Suzuki, Takashi, Yasuhiro Miki, Yasuhiro Nakamura, Takuya Moriya, Kiyoshi Ito, Noriaki Ohuchi, and Hironobu Sasano. "Sex steroid-producing enzymes in human breast cancer." Endocrine-Related Cancer 12, no. 4 (December 2005): 701–20. http://dx.doi.org/10.1677/erc.1.00834.

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It is well known that sex steroids are involved in the growth of breast cancers, and the great majority of breast carcinomas express estrogen (ER), progesterone (PR), and androgen (AR) receptors. In particular, recent studies have demonstrated that estrogens and androgens are locally produced in breast carcinoma tissues, and total blockade of in situ estrogen production potentially leads to an improvement in prognosis of breast cancer patients. Therefore, it is important to obtain a better understanding of sex steroid-producing enzymes in breast carcinoma tissues. In this review, we summarize recent studies on the expression and regulation of enzymes related to intratumoral production of estrogens (aromatase, 17β-hydroxysteroid dehydrogenase type 1 (17βHSD1), and steroid sulfatase (STS) etc) and androgens (17βHSD5 and 5α-reductase) in human breast carcinoma tissues, and discuss the biological and/or clinical significance of these enzymes. The cellular localization of aromatase in breast carcinoma tissues still remains controversial. Therefore, we examined localization of aromatase mRNA in breast carcinoma tissues by laser capture microdissection/real time-polymerase chain reaction. Aromatase mRNA expression was detected in both carcinoma and intratumoral stromal cells, and the expression level of aromatase mRNA was higher in intratumoral stromal cells than in carcinoma cells in the cases examined. We also examined an association among the immunoreactivity of enzymes related to intratumoral estrogen production and ERs in breast carcinoma tissues, but no significant association was detected. Therefore, the enzymes responsible for the intratumoral production of estrogen may not always be the same among breast cancer patients, and not only aromatase but also other enzymes such as STS and 17βHSD1 may have important therapeutic potential as targets for endocrine therapy in breast cancer patients.

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Adnan Yasseen, Hadeel, Rawand Tajuldeen Sahib, and Shaho Abdulrehman Ezzaddin. "MITOCHONDRIAL ENZYMES CORRELATION WITH BREAST CANCER CLINICOPATHOLOGICAL PARAMETERS/ A STUDY IN SULAIMANI CITY-IRAQ." Journal of Sulaimani Medical College 8, no. 1 (April 15, 2018): 37–46. http://dx.doi.org/10.17656/jsmc.10149.

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Wiebe, John P. "Progesterone metabolites in breast cancer." Endocrine-Related Cancer 13, no. 3 (September 2006): 717–38. http://dx.doi.org/10.1677/erc.1.01010.

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In the 70 years since progesterone (P) was identified in corpus luteum extracts, its metabolism has been examined extensively in many tissues and cell lines from numerous species. In addition to the reproductive tissues and adrenals, every other tissue that has been investigated appears to have one or more P-metabolizing enzyme, each of which is specific for a particular site on the P molecule. In the past, the actions of the P metabolizing enzymes generally have been equated to a means of reducing the P concentration in the tissue microenvironment, and the products have been dismissed as inactive waste metabolites. In human breast tissues and cell lines, the following P-metabolizing enzymes have been identified: 5α-reductase, 3α-hydroxysteroid oxidoreductase (3α-HSO), 3β-HSO, 20α-HSO, and 6α-hydroxylase. Rather than providing diverse pathways for inactivating and controlling the concentration of P in breast tissue microenvironments, it is proposed that the enzymes act directly on P to produce two types of autocrines/paracrines with opposing regulatory roles in breast cancer. Evidence is reviewed which shows that P is directly converted to the 4-pregnenes, 3α-hydroxy-4-pregnen-20-one (3α-dihydroprogesterone; 3αHP) and 20α-dihydroprogesterone (20αHP), by the actions of 3α-HSO and 20α-HSO respectively and to the 5α-pregnane, 5α-pregnane-3,20-dione(5α-dihydroprogesterone; 5αP), by the irreversible action of 5α-reductase. In vitro studies on a number of breast cell lines indicate that 3αHP promotes normalcy by downregulating cell proliferation and detachment, whereas 5αP promotes mitogenesis and metastasis by stimulating cell proliferation and detachment. The hormones bind to novel, separate, and specific plasma membrane-based receptors and influence opposing actions on mitosis, apoptosis, and cytoskeletal and adhesion plaque molecules via cell signaling pathways. In normal tissue, the ratio of 4-pregnenes:5α-pregnanes is high because of high P 3α- and 20α-HSO activities/expression and low P 5α-reductase activity/expression. In breast tumor tissue and tumorigenic cell lines, the ratio is reversed in favor of the 5α-pregnanes because of altered P-metabolizing enzyme activities/expression. The evidence suggests that the promotion of breast cancer is related to changes in in situ concentrations of cancer-inhibiting and -promoting P metabolites. Current estrogen-based theories and therapies apply to only a fraction of all breast cancers; the majority (about two-thirds) of breast cancer cases are estrogen-insensitive and have lacked endocrine explanations. As the P metabolites, 5αP and 3αHP, have been shown to act with equal efficacy on all breast cell lines tested, regardless of their tumorigenicity, estrogen sensitivity, and estrogen receptor/progesterone receptor status, it is proposed that they offer a new hormonal basis for all forms of breast cancer. New diagnostic and therapeutic possibilities for breast cancer progression, control, regression, and prevention are suggested.

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Raza, Uzma, Aziza Khannum, and Shahnawaz Jamali. "LIVER ENZYMES." Professional Medical Journal 22, no. 06 (June 10, 2015): 745–51. http://dx.doi.org/10.29309/tpmj/2015.22.06.1242.

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Objective: To study the effect of breast cancer treatment on liver enzymes indiabetic and cardiac breast cancer females. Study Design: Cross-sectional type of study.Setting: Liaquat National Hospital Karachi. Period: January 2008 to January 2010. Patientsand Methods: Total 47 breast cancer patients. Out of these, 22 were diabetic and 25 werecardiac patients, visiting the oncology OPD of the hospital. Patients with metastasis to distantorgans were excluded from the study. Treatment was carried under the supervision of anoncologist. Samples were collected twice during the study. First sample was collected at diseasepresentation before starting any type of treatment and second time, sample was collected14 weeks after the last chemotherapy dose. Statistical analysis: Data was analyzed usingstatistical package (SPSS version 11.0). “Students t-test”and analysis of variance (ANOVA) wasused to analyze the means and standard deviations of quantitative/continuous variables. Inall statistical analysis p<0.05 was considered significant. Results: In all patient groups aftertreatment alkaline phosphatase was significantly high as compared to that before treatment(p<0.05) whereas alanine transaminase increased significantly without including Tamoxifenin the treatment. Variation pattern of liver enzyme was the same in both patient groups.Conclusions: Altered profile of liver enzyme was similar in both patient groups therefor thevariations cannot be attributed to hyperglycemia in diabetic females and the alterations in liverenzymes were attributed to liver damage by chemotherapy and fatty infiltration of liver inducedby Tamoxifen.

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Brueggemeier, Robert W., Jeanette A. Richards, and Trevor A. Petrel. "Aromatase and cyclooxygenases: enzymes in breast cancer." Journal of Steroid Biochemistry and Molecular Biology 86, no. 3-5 (September 2003): 501–7. http://dx.doi.org/10.1016/s0960-0760(03)00380-7.

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Tappel, Al. "Lysosomal enzymes and initiation of breast cancer." Medical Hypotheses 64, no. 2 (January 2005): 288–89. http://dx.doi.org/10.1016/j.mehy.2004.07.025.

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Jansson, Agneta. "17Beta-hydroxysteroid dehydrogenase enzymes and breast cancer." Journal of Steroid Biochemistry and Molecular Biology 114, no. 1-2 (March 2009): 64–67. http://dx.doi.org/10.1016/j.jsbmb.2008.12.012.

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Wang, Shu-Ching M., Dennis H. Dowhan, and George E. O. Muscat. "Epigenetic arginine methylation in breast cancer: emerging therapeutic strategies." Journal of Molecular Endocrinology 62, no. 3 (April 2019): R223—R237. http://dx.doi.org/10.1530/jme-18-0224.

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Breast cancer is a heterogeneous disease, and the complexity of breast carcinogenesis is associated with epigenetic modification. There are several major classes of epigenetic enzymes that regulate chromatin activity. This review will focus on the nine mammalian protein arginine methyltransferases (PRMTs) and the dysregulation of PRMT expression and function in breast cancer. This class of enzymes catalyse the mono- and (symmetric and asymmetric) di-methylation of arginine residues on histone and non-histone target proteins. PRMT signalling (and R methylation) drives cellular proliferation, cell invasion and metastasis, targeting (i) nuclear hormone receptor signalling, (ii) tumour suppressors, (iii) TGF-β and EMT signalling and (iv) alternative splicing and DNA/chromatin stability, influencing the clinical and survival outcomes in breast cancer. Emerging reports suggest that PRMTs are also implicated in the development of drug/endocrine resistance providing another prospective avenue for the treatment of hormone resistance and associated metastasis. The complexity of PRMT signalling is further underscored by the degree of alternative splicing and the scope of variant isoforms (with distinct properties) within each PRMT family member. The evolution of PRMT inhibitors, and the ongoing clinical trials of PRMT inhibitors against a subgroup of solid cancers, coupled to the track record of lysine methyltransferases inhibitors in phase I/II clinical trials against cancer underscores the potential therapeutic utility of targeting PRMT epigenetic enzymes to improve survival outcomes in aggressive and metastatic breast cancer.

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Makar, Subhajit, Abhrajyoti Ghosh, Ashok Kumar, and Sushil K. Singh. "Recent Studies on Aromatase and Sulfatase Involved in Breast Cancer and their Inhibitors." Current Enzyme Inhibition 16, no. 1 (May 4, 2020): 20–44. http://dx.doi.org/10.2174/1573408016666200325120248.

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Enzyme aromatase uses several androgen substrates for the biosynthesis of estrogen, i.e. conversion of androstenedione to estrone and testosterone to biologically potent estradiol. Aromatase inhibitors (AIs) such as anastrozole, letrozole and exemestane have been established in standard endocrine therapy of breast cancer, by interfering with estrogen signaling cascade. Steroid sulphatase (STS) regulates the level of active oestrogens and androgens in human target organs and steroidogenic tissues, which have a key role in hormone dependent breast cancers (HDBC). Sulfatase is still under the exploration stage and is yet to emerge as a potential therapeutic target in breast cancer. The discovery of estrone 3-O-sulfamate (EMATE), a highly potent irreversible STS inhibitor, accelerated the development of potent steroidal and nonsteroidal STS inhibitors. Attempts are also being made for the development of dual inhibitors of AI and STS, as an alternative approach to overcome the acquired resistance. This review includes the molecular structures and biochemistry of aromatase and sulphatase enzymes. The advances in the development of inhibitors of the two enzymes have also been outlined.

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Çelik, V. Kenan, Sercan Kapancık, Turgut Kaçan, Selen Baloglu Kaçan, Serkan Kapancık, and Hasan Kılıçgün. "Serum levels of polyamine synthesis enzymes increase in diabetic patients with breast cancer." Endocrine Connections 6, no. 8 (November 2017): 574–79. http://dx.doi.org/10.1530/ec-17-0137.

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Background In this study, it was aimed to investigate the relationship between diabetes and breast cancer and the detection of enzymes and ornithine levels in polyamine synthesis pathway in diabetes, breast cancer and diabetic breast cancer patients. Methods Ornithine, arginine decarboxylase, ornithine decarboxylase and agmatinase levels have been measured in serum of all groups. Ornithine levels were measured spectrophotometrically. Arginine decarboxylase, ornithine decarboxylase and agmatinase levels were determined by ELISA kits. Results Except for the diabetic group, the levels of enzymes in the polyamine synthesis pathway were increased in all and statistically significant (P < 0.05). The increase in the levels of agmatinase was very important among the enzymes (P < 0.001). Conclusions Decreased levels of polyamine synthase enzymes in diabetes mellitus were found to be increased patients with breast cancer. Whether and how diabetes-based breast cancer development relates to increase activity of enzymes responsible for polyamine synthesis requires further mechanistic and prospective monitoring studies in larger patient cohorts.

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Hennipman, A., J. Smits, B. van Oirschot, J. C. van Houwelingen, G. Rijksen, J. P. Neyt, J. A. M. van Unnik, and G. E. J. Staal. "Glycolytic Enzymes in Breast Cancer, Benign Breast Disease and Normal Breast Tissue." Tumor Biology 8, no. 5 (1987): 251–63. http://dx.doi.org/10.1159/000217529.

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Perestrelo, Rosa, Marijana Petkovic, and Catarina Luís Silva. "Analytical Platforms for the Determination of Phospholipid Turnover in Breast Cancer Tissue: Role of Phospholipase Activity in Breast Cancer Development." Metabolites 11, no. 1 (January 4, 2021): 32. http://dx.doi.org/10.3390/metabo11010032.

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Altered lipid metabolism has been associated with the progression of various cancers, and aberrant expression of enzymes involved in the lipid metabolism has been detected in different stages of cancer. Breast cancer (BC) is one of the cancer types known to be associated with alterations in the lipid metabolism and overexpression of enzymes involved in this metabolism. It has been demonstrated that inhibition of the activity of certain enzymes, such as that of phospholipase A2 in BC cell lines sensitizes these cells and decreases the IC50 values for forthcoming therapy with traditional drugs, such as doxorubicin and tamoxifen. Moreover, other phospholipases, such as phospholipase C and D, are involved in intracellular signal transduction, which emphasizes their importance in cancer development. Finally, BC is assumed to be dependent on the diet and the composition of lipids in nutrients. Despite their importance, analytical approaches that can associate the activity of phospholipases with changes in the lipid composition and distribution in cancer tissues are not yet standardized. In this review, an overview of various analytical platforms that are applied on the study of lipids and phospholipase activity in BC tissues will be given, as well as their association with cancer diagnosis and tumor progression. The methods that are applied to tissues obtained from the BC patients will be emphasized and critically evaluated, regarding their applicability in oncology.

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Harrington, William R., Surojeet Sengupta, and Benita S. Katzenellenbogen. "Estrogen Regulation of the Glucuronidation Enzyme UGT2B15 in Estrogen Receptor-Positive Breast Cancer Cells." Endocrinology 147, no. 8 (August 1, 2006): 3843–50. http://dx.doi.org/10.1210/en.2006-0358.

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Estrogens and androgens influence many properties of breast cancer cells; hence, regulation of local estrogen and androgen levels by enzymes involved in steroid hormone biosynthesis and metabolism would impact signaling by these hormones in breast cancer cells. In this study, we show that the UDP-glucuronosyltransferase (UGT) enzyme UGT2B15, a member of the UGT family of phase II enzymes involved in the glucuronidation of steroids and xenobiotics, is a novel, estrogen-regulated gene in estrogen receptor (ER)-positive human breast cancer cells (MCF-7, BT474, T47D, and ZR-75). UGT2B15 is the only UGT2B enzyme up-regulated by estrogen, and marked estradiol stimulation of UGT2B15 mRNA levels is observed, in a time- and dose-dependent manner. UGT2B15 stimulation by estradiol is blocked by the antiestrogen ICI182,780, but not by the translational inhibitor cycloheximide, indicating that UGT2B15 is likely a primary transcriptional response mediated through the ER. UGT2B15 up-regulation is also evoked by other estrogens (propylpyrazoletriol, genistein) and by the androgen 5α-dihydrotestosterone working through the ER, but not by other steroid hormone receptor ligands. Western blot and immunocytochemical analyses with several UGT2B-specific antibodies we have designed and steroid glucuronidation assays indicate a large increase in both cellular UGT2B15 protein and enzyme activity after estrogen treatment. Due to the important role of UGT enzymes in forming conjugates between steroids and glucuronic acid, thereby inactivating them and targeting them for removal, the estrogen-induced up-regulation of UGT2B15 might have a significant moderating effect on estrogen and androgen concentrations, thereby reducing their signaling in breast cancer cells.

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Kharitonov, S., A. Zikiriahodzhaev, M. Ermoshchenkova, A. Sukhot’ko, M. Fedorova, E. Pudova, B. Alekseev, A. Kaprin, and A. Kudryavtseva. "HEXOKINASES IN BREAST CANCER." International Journal of Biosciences and Biotechnology 4, no. 2 (April 2, 2017): 110. http://dx.doi.org/10.24843/ijbb.2017.v04.i02.p05.

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Hexokinases are one of the key enzymes involved in the process of glycolysis. The level of expression of hexokinases is widely studied in breast cancer as a possible marker of unfavorable prognosis and aggressiveness of tumors. The level of expression of hexokinase may reflect the level of glycolysis activation and, thus, indicate samples with the most altered cellular metabolism.

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Qattan, Amal. "Metabolic Reprogramming of Triple-Negative Breast Cancer: The Role of miRNAs." microRNA Diagnostics and Therapeutics 3, no. 1 (December 20, 2017): 1–8. http://dx.doi.org/10.1515/micrnat-2017-0001.

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AbstractMicroRNAs (miRNAs) are well known to influence the expression of the genes that regulate critical cellular functions. Various reports have suggested that they play critical roles in breast cancer metabolism through the regulation of various metabolic pathways, including the metabolism of glucose, lipids, glycolysis and the mitochondrial tricarboxylic acid cycle (TCA). miRNAs regulate the metabolic process by targeting key molecules (enzymes, kinases transporters) or by modifying the expression of key transcription molecules. In addition, miRNAs can indirectly regulate mRNA translation by targeting chromatin-remodeling enzymes. Furthermore, miRNAs influence the expression of both oncogenes and tumor suppressors and have a major impact on PI3K/AKT, HIF, and MYC signal transduction, which contributes to the metabolic phenotype in human cancer. Although human epidermal growth factor and endocrine therapies have been effective in treating breast cancer, for locally advanced and distant metastases mortality remains high. Drug resistance and recurrence remain major hurdles for advanced breast cancer therapy. Given the critical influence of metabolic reprogramming in the progression of neoplasm, tumorigenesis and metastasis, research should focus on novel targets of metabolic enzymes to reverse drug resistance and improve overall survival rates. Blocking the miRNAs that contribute to metabolic reprogramming or the use of exogenous miRNAs as antisense oligonucleotides, may be an effective way to treat aggressive, chemo-resistant cancers. This review summarizes current knowledge on the mechanism of action of miRNAs in altering the metabolism of cancer cells and presents possible therapeutic approaches to treating breast cancers that are resistant to current drugs.

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Jones, Wilson, Thomas, Gaughan, and Wade. "The Histone Demethylase Enzymes KDM3A and KDM4B Co-Operatively Regulate Chromatin Transactions of the Estrogen Receptor in Breast Cancer." Cancers 11, no. 8 (August 6, 2019): 1122. http://dx.doi.org/10.3390/cancers11081122.

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Many estrogen receptor (ER)-positive breast cancers develop resistance to endocrine therapy but retain canonical receptor signalling in the presence of selective ER antagonists. Numerous co-regulatory proteins, including enzymes that modulate the chromatin environment, control the transcriptional activity of the ER. Targeting ER co-regulators has therefore been proposed as a novel therapeutic approach. By assessing DNA-binding dynamics in ER-positive breast cancer cells, we have identified that the histone H3 lysine 9 demethylase enzymes, KDM3A and KDM4B, co-operate to regulate ER activity via an auto-regulatory loop that facilitates the recruitment of each co-activating enzyme to chromatin. We also provide evidence that suggests that KDM3A primes chromatin for deposition of the ER pioneer factor FOXA1 and recruitment of the ER-transcriptional complex, all prior to ER recruitment, therefore establishing an important mechanism of chromatin regulation involving histone demethylases and pioneer factors, which controls ER functionality. Importantly, we show via global gene-expression analysis that a KDM3A/KDM4B/FOXA1 co-regulated gene signature is enriched for pro-proliferative and ER-target gene sets, suggesting that abrogation of this network could be an efficacious therapeutic strategy. Finally, we show that depletion of both KDM3A and KDM4B has a greater inhibitory effect on ER activity and cell growth than knockdown of each individual enzyme, suggesting that targeting both enzymes represents a potentially efficacious therapeutic option for ER-driven breast cancer.

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Tandi, Dipty. "TNBC: A brief discussion on Triple Negative Breast Cancer." International Journal of Advanced Multidisciplinary Research 8, no. 6 (June 30, 2021): 75–82. http://dx.doi.org/10.22192/ijamr.2021.08.06.006.

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TNBC; Triple negative breast cancer is one of the most aggressive type of breast cancer with a high reoccurrence and mortality rate. The reason behind its aggressive type is that TNBC do not have such specific receptors as other cancers. Substantially, Breast tumor cells carries receptors that work as doors for many mechanisms and hormone/enzyme based treatment. These receptors are estrogen (female hormone), Progesterone (female hormone) and HER-2 (Protein; Human epidermal receptor). Absence of these enzymes is result into the less option availability in cancer treatment. To find more possible treatments like chemotherapy, lumpectomy, radiation therapy and other gene therapy we first need to understand the concept behind occurrence and reoccurrence of TNBC. This review listed the possible study of triple negative breast cancer including its appearance in society and the molecular/genetic involvement. It is formerly known that cancer take place due to mutation in BRCA group of genes so it is important to know how it works in the case of TNBC. This study also summarizes the influence of anti-diabetic drug treatment (e.g. metformin) on diabetic cancer patients in order to cancer therapy of TNBC and effect of high glucose concentric cells on anti- cancer drug treatments and strategies for development in TNBC development. Keywords: TNBC; female hormone, breast cancer, BRCA group.

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Murray, Graeme I., Richard J. Weaver, Pamela J. Paterson, Stanley W. B. Ewen, William T. Melvin, and M. Burke Danny. "Expression of xenobiotic metabolizing enzymes in breast cancer." Journal of Pathology 169, no. 3 (March 1993): 347–53. http://dx.doi.org/10.1002/path.1711690312.

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Šarmanová, Jana, Simona Šůsová, Ivan Gut, Marcela Mrhalová, Roman Kodet, Jan Adámek, Zdeněk Roth, and Pavel Souček. "Breast cancer: role of polymorphisms in biotransformation enzymes." European Journal of Human Genetics 12, no. 10 (July 28, 2004): 848–54. http://dx.doi.org/10.1038/sj.ejhg.5201249.

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Rice, Suman, and Saffron A. Whitehead. "Phytoestrogens and breast cancer –promoters or protectors?" Endocrine-Related Cancer 13, no. 4 (December 2006): 995–1015. http://dx.doi.org/10.1677/erc.1.01159.

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The majority of breast cancers are oestrogen dependent and in postmenopausal women the supply of oestrogens in breast tissue is derived from the peripheral conversion of circulating androgens. There is, however, a paradox concerning the epidemiology of breast cancer and the dietary intake of phytoestrogens that bind weakly to oestrogen receptors and initiate oestrogen-dependent transcription. In Eastern countries, such as Japan, the incidence of breast cancer is approximately one-third that of Western countries whilst their high dietary intake of phytoestrogens, mainly in the form of soy products, can produce circulating levels of phytoestrogens that are known experimentally to have oestrogenic effects. Indeed, their weak oestrogenicity has been used to advantage by herbalist medicine to promote soy products as a natural alternative to conventional hormone replacement therapy (HRT). Such usage could increase in light of recent evidence that long-term HRT usage may be associated with an increased risk of breast cancer with a consequent reduction in prescription rates. So, are phytoestrogens safe as a natural alternative to HRT and could they be promoters or protectors of breast cancer? If they are promoters, then we must assume that it is due to their oestrogenic effect. If they are protectors, then other actions of phytoestrogens, including their ability to inhibit enzymes that are responsible for converting androgens and weak oestrogens into oestradiol, must be considered. This paper addresses these questions by reviewing the actions of phytoestrogens on oestrogen receptors and key enzymes that convert androgens to oestrogens in relation to the growth of breast cancer cells. In addition, it compares the experimental and epidemiological evidence pertinent to the potential beneficial or harmful effects of phytoestrogens in relation to the incidence/progression of breast cancer and their efficacy as natural alternatives to conventional HRT.

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Simeone, Pasquale, Stefano Tacconi, Serena Longo, Paola Lanuti, Sara Bravaccini, Francesca Pirini, Sara Ravaioli, Luciana Dini, and Anna M. Giudetti. "Expanding Roles of De Novo Lipogenesis in Breast Cancer." International Journal of Environmental Research and Public Health 18, no. 7 (March 30, 2021): 3575. http://dx.doi.org/10.3390/ijerph18073575.

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In recent years, lipid metabolism has gained greater attention in several diseases including cancer. Dysregulation of fatty acid metabolism is a key component in breast cancer malignant transformation. In particular, de novo lipogenesis provides the substrate required by the proliferating tumor cells to maintain their membrane composition and energetic functions during enhanced growth. However, it appears that not all breast cancer subtypes depend on de novo lipogenesis for fatty acid replenishment. Indeed, while breast cancer luminal subtypes rely on de novo lipogenesis, the basal-like receptor-negative subtype overexpresses genes involved in the utilization of exogenous-derived fatty acids, in the synthesis of triacylglycerols and lipid droplets, and fatty acid oxidation. These metabolic differences are specifically associated with genomic and proteomic changes that can perturb lipogenic enzymes and related pathways. This behavior is further supported by the observation that breast cancer patients can be stratified according to their molecular profiles. Moreover, the discovery that extracellular vesicles act as a vehicle of metabolic enzymes and oncometabolites may provide the opportunity to noninvasively define tumor metabolic signature. Here, we focus on de novo lipogenesis and the specific differences exhibited by breast cancer subtypes and examine the functional contribution of lipogenic enzymes and associated transcription factors in the regulation of tumorigenic processes.

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Yeshowardhana, M. M. Gupta, Geeta Bansal, Sindhu Goyal, V. S. Singh, and Km Sangita Jain. "Serum Glycolytic Enzymes in Breast Carcinoma." Tumori Journal 72, no. 1 (February 1986): 35–41. http://dx.doi.org/10.1177/030089168607200106.

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Nguyen, Yen T. K., Joon Sung Park, Jun Young Jang, Kyung Rok Kim, Tam T. L. Vo, Kyu-Won Kim, and Byung Woo Han. "Structural and Functional Analyses of Human ChaC2 in Glutathione Metabolism." Biomolecules 10, no. 1 (December 24, 2019): 31. http://dx.doi.org/10.3390/biom10010031.

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Glutathione (GSH) degradation plays an essential role in GSH homeostasis, which regulates cell survival, especially in cancer cells. Among human GSH degradation enzymes, the ChaC2 enzyme acts on GSH to form 5-l-oxoproline and Cys-Gly specifically in the cytosol. Here, we report the crystal structures of ChaC2 in two different conformations and compare the structural features with other known γ-glutamylcyclotransferase enzymes. The unique flexible loop of ChaC2 seems to function as a gate to achieve specificity for GSH binding and regulate the constant GSH degradation rate. Structural and biochemical analyses of ChaC2 revealed that Glu74 and Glu83 play crucial roles in directing the conformation of the enzyme and in modulating the enzyme activity. Based on a docking study of GSH to ChaC2 and binding assays, we propose a substrate-binding mode and catalytic mechanism. We also found that overexpression of ChaC2, but not mutants that inhibit activity of ChaC2, significantly promoted breast cancer cell proliferation, suggesting that the GSH degradation by ChaC2 affects the growth of breast cancer cells. Our structural and functional analyses of ChaC2 will contribute to the development of inhibitors for the ChaC family, which could effectively regulate the progression of GSH degradation-related cancers.

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Liu, Sitong, Lichun Wang, Dongjun Jiang, Wei Wei, Mushyeda Fatima Nasir, Muhammad Saad Khan, Qudsia Yousafi, et al. "Sumoylation as an Emerging Target in Therapeutics against Cancer." Current Pharmaceutical Design 26, no. 37 (October 26, 2020): 4764–76. http://dx.doi.org/10.2174/1381612826666200622124134.

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Sumoylation is the Post-translational modification gaining most of the research interest recently. Sumoylation is involved in various crucial functions of the cell such as regulation of cell cycle, DNA damage repair, apoptosis, etc. Oncology is advancing in radiotherapy, targeted chemotherapy, various forms of immunotherapy and targeted gene therapy. Researches are being conducted to prove its connotation with a variety of cancers and inhibitors are being developed to obstruct the fatal effect caused by misbalance of the SUMO-catalytic cycle. It has been shown that up-regulation of certain enzymes of Sumoylation correlates with cancer incidence in most of the cases. However, in some cases, down-regulation also associates with cancer invasion such as underexpression of UBC9 in initial stage breast cancer. This can aid in future study, treatment, and diagnosis of a variety of cancers including breast cancer, prostate cancer, lung adenocarcinoma, melanoma, multiple myeloma, etc. Various mechanistic assays are being developed and used to identify potential inhibitors against the dysregulated proteins of Sumoylation. This review summarizes the normal roles of the enzymes involved in the SUMOcatalytic cycle, their misbalanced regulation leading to tumorigenesis and nearly all the potent inhibitors identified to date, while after detailed studied it was observed that ML-792 could be a promising inhibitor in treating cancers by inhibiting Sumoylation enzymes.

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Duffy, M. J. "Biochemical markers as prognostic indices in breast cancer." Clinical Chemistry 36, no. 2 (February 1, 1990): 188–91. http://dx.doi.org/10.1093/clinchem/36.2.188.

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Abstract Traditional prognostic markers in breast cancer include histological variables such as tumor size, grade, and axillary node status. In recent years some new potential prognostic markers of a biochemical nature have been described: estradiol receptors, progesterone receptors, epidermal growth factor receptors, erbB-2 proto-oncogene, and certain proteolytic enzymes. None of these new markers excels axillary node status as a prognostic marker. Biochemical markers can, however, be evaluated with use of minimal surgery and may help distinguish the minority of aggressive axillary-node-negative breast cancers.

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Shackelford, Rodney E., Islam Z. Mohammad, Andrew T. Meram, David Kim, Fawaz Alotaibi, Stavan Patel, Ghali E. Ghali, and Christopher G. Kevil. "Molecular Functions of Hydrogen Sulfide in Cancer." Pathophysiology 28, no. 3 (September 20, 2021): 437–56. http://dx.doi.org/10.3390/pathophysiology28030028.

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Hydrogen sulfide (H2S) is a gasotransmitter that exerts a multitude of functions in both physiologic and pathophysiologic processes. H2S-synthesizing enzymes are increased in a variety of human malignancies, including colon, prostate, breast, renal, urothelial, ovarian, oral squamous cell, and thyroid cancers. In cancer, H2S promotes tumor growth, cellular and mitochondrial bioenergetics, migration, invasion, angiogenesis, tumor blood flow, metastasis, epithelia–mesenchymal transition, DNA repair, protein sulfhydration, and chemotherapy resistance Additionally, in some malignancies, increased H2S-synthesizing enzyme expression correlates with a worse prognosis and a higher tumor stage. Here we review the role of H2S in cancer, with an emphasis on the molecular mechanisms by which H2S promotes cancer development, progression, dedifferentiation, and metastasis.

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Lange, Carol A., and Douglas Yee. "Progesterone and Breast Cancer." Women's Health 4, no. 2 (March 2008): 151–62. http://dx.doi.org/10.2217/17455057.4.2.151.

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Progesterone is an ovarian steroid hormone that is essential for normal breast development during puberty and in preparation for lactation and breastfeeding. The actions of progesterone are primarily mediated by its high-affinity receptors, which include the classical progesterone receptor (PR)-A and -B isoforms, located in diverse tissues, including the brain, where progesterone controls reproductive behavior, and the breast and reproductive organs. Progestins are frequently prescribed for contraception or during postmenopausal hormone replacement therapy, in which progestins are combined with estrogen as a means to block estrogen-induced endometrial growth. The role of estrogen as a potent breast mitogen is undisputed, and inhibitors of the estrogen receptor and estrogen-producing enzymes (aromatases) are effective first-line cancer therapies. However, PR action in breast cancer is grossly understudied and remains controversial. Herein, we review existing evidence and discuss the challenges to defining a role for progesterone in breast cancer.

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Zmorzyński, Szymon, Grażyna Świderska-Kołacz, Dorota Koczkodaj, and Agata Anna Filip. "Significance of Polymorphisms and Expression of Enzyme-Encoding Genes Related to Glutathione in Hematopoietic Cancers and Solid Tumors." BioMed Research International 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/853573.

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Antioxidant compounds such as glutathione and its enzymes have become the focus of attention of medical sciences. Glutathione, a specific tripeptide, is involved in many intercellular processes. The glutathione concentration is determined by the number of GAG repeats in gamma-glutamylcysteine synthetase. GAG polymorphisms are associated with an increased risk of schizophrenia, berylliosis, diabetes, lung cancer, and nasopharyngeal tumors. Cancer cells with high glutathione concentration are resistant to chemotherapy treatment. The oxidized form of glutathione is formed by glutathione peroxidases (GPXs). The changes in activity of GPX1, GPX2, and GPX3 isoforms may be associated with the development of cancers, for example, prostate cancer or even colon cancer. Detoxification of glutathione conjugates is possible due to activity of glutathione S-transferases (GSTs). Polymorphisms in GSTM1, GSTP1, and GSTO1 enzymes increase the risk of developing breast cancer and hepatocellular carcinoma. Gamma-glutamyl transpeptidases (GGTs) are responsible for glutathione degradation. Increased activity of GGT correlates with adverse prognosis in patients with breast cancer. Studies on genes encoding glutathione enzymes are continued in order to determine the correlation between DNA polymorphisms in cancer patients.

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Dunn, Barbara K., D. Lawrence Wickerham, and Leslie G. Ford. "Prevention of Hormone-Related Cancers: Breast Cancer." Journal of Clinical Oncology 23, no. 2 (January 10, 2005): 357–67. http://dx.doi.org/10.1200/jco.2005.08.028.

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Carcinogenesis in the breast is a hormonally dependent process. Evidence implicating estrogen as a key breast carcinogen comes from various lines of investigation. Traditional epidemiologic studies demonstrate associations between estrogen exposure, both exogenous and endogenous, and increased breast cancer risk. Ongoing genetic epidemiologic studies also show associations between specific polymorphisms in estrogen-metabolizing genes and risk, albeit inconsistently. The application of these findings to the treatment and, more recently, the prevention of breast cancer has led to the development of agents that either (1) inhibit estrogen action at the estrogen receptor (selective estrogen receptor modulators (SERMs]); or (2) inhibit estrogen-synthesizing enzymes, thereby abrogating synthesis of this hormone (aromatase inhibitors). Large phase III trials have evaluated the ability of such agents to reduce the incidence of breast cancer in women at increased risk of the disease. The National Surgical Adjuvant Breast and Bowel Project (NSABP) P-1: Breast Cancer Prevention Trial (BCPT) demonstrated the superiority of the SERM tamoxifen to placebo in reducing breast cancer risk, leading to the Food and Drug Administration approval of tamoxifen for risk reduction. The implementation of tamoxifen for this indication has not become widespread in clinical practice, however, for a variety of reasons that we discuss. Results from the NSABP Study of Tamoxifen and Raloxifene, which compares the risk-reducing efficacy as well as toxicity of these two SERMs in a similar high-risk population, will be available in the near future. Based on promising data involving reduction of contralateral breast cancer risk in adjuvant studies, several aromatase inhibitors, including letrozole, anastrozole, and exemestane, are being incorporated into trials evaluating their efficacy as preventive agents in women at increased risk.

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Purwaha, Preeti, Franklin Gu, Danthasinghe Piyarathna, Theckelnaycke Rajendiran, Anindita Ravindran, Angela Omilian, Sao Jiralerspong, et al. "Unbiased Lipidomic Profiling of Triple-Negative Breast Cancer Tissues Reveals the Association of Sphingomyelin Levels with Patient Disease-Free Survival." Metabolites 8, no. 3 (July 13, 2018): 41. http://dx.doi.org/10.3390/metabo8030041.

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The reprogramming of lipid metabolism is a hallmark of many cancers that has been shown to promote breast cancer progression. While several lipid signatures associated with breast cancer aggressiveness have been identified, a comprehensive lipidomic analysis specifically targeting the triple-negative subtype of breast cancer (TNBC) may be required to identify novel biomarkers and therapeutic targets for this most aggressive subtype of breast cancer that still lacks effective therapies. In this current study, our global LC-MS-based lipidomics platform was able to measure 684 named lipids across 15 lipid classes in 70 TNBC tumors. Multivariate survival analysis found that higher levels of sphingomyelins were significantly associated with better disease-free survival in TNBC patients. Furthermore, analysis of publicly available gene expression datasets identified that decreased production of ceramides and increased accumulation of sphingoid base intermediates by metabolic enzymes were associated with better survival outcomes in TNBC patients. Our LC-MS lipidomics profiling of TNBC tumors has, for the first time, identified sphingomyelins as a potential prognostic marker and implicated enzymes involved in sphingolipid metabolism as candidate therapeutic targets that warrant further investigation.

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Thomas, Patricia A., Dilek Oykutlu, Bel Pou, Denise Tyler, Larry W. Oberley, Robert A. Robinson, and Julia C. Lenel. "Immunohistochemical characterization of antioxidant enzymes in human breast cancer." Pathology & Oncology Research 3, no. 4 (December 1997): 278–86. http://dx.doi.org/10.1007/bf02904287.

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Špačková, Jitka, Klára Gotvaldová, Aleš Dvořák, Alexandra Urbančoková, Kateřina Pospíšilová, David Větvička, Alberto Leguina-Ruzzi, et al. "Biochemical Background in Mitochondria Affects 2HG Production by IDH2 and ADHFE1 in Breast Carcinoma." Cancers 13, no. 7 (April 4, 2021): 1709. http://dx.doi.org/10.3390/cancers13071709.

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Mitochondrial production of 2-hydroxyglutarate (2HG) can be catalyzed by wild-type isocitrate dehydrogenase 2 (IDH2) and alcohol dehydrogenase, iron-containing 1 (ADHFE1). We investigated whether biochemical background and substrate concentration in breast cancer cells promote 2HG production. To estimate its role in 2HG production, we quantified 2HG levels and its enantiomers in breast cancer cells using analytical approaches for metabolomics. By manipulation of mitochondrial substrate fluxes using genetic and pharmacological approaches, we demonstrated the existence of active competition between 2HG producing enzymes, i.e., IDH2 and ADHFE1. Moreover, we showed that distinct fractions of IDH2 enzyme molecules operate in distinct oxido-reductive modes, providing NADPH and producing 2HG simultaneously. We have also detected 2HG release in the urine of breast cancer patients undergoing adjuvant therapy and detected a correlation with stages of breast carcinoma development. In summary, we provide a background for vital mitochondrial production of 2HG in breast cancer cells with outcomes towards cancer biology and possible future diagnosis of breast carcinoma.

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Veropotvelyan, P. N., I. S. Tsekhmistrenko, N. P. Veropotvelyan, S. P. Yaruchik, and I. V. Stepanovich. "Breast cancer in reproductive age, inducers of risk and the role of vitamin D." HEALTH OF WOMAN, no. 9(115) (November 30, 2016): 103–11. http://dx.doi.org/10.15574/hw.2016.115.103.

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The article presents the inductors risk of developing breast cancer (RGI). Сonsidering the risks of breast cancer in women in different age periods, appropriate use of targeted cancer protector and symptomatic therapy. Gene polymorphism of the vitamin D, the different expression of enzymes involved in the synthesis of biologically active forms of vitamin D and catabolism of vitamin ultimately determine the local concentration of the vitamin D. the Latter regulates the proliferation of breast cells which is the basis of benign lesions and cancer of the breast. Timely correction of vitamin D deficiency is one of the most effective methods for primary prevention of breast cancer. Key words: breast cancer, inductors risk of breast cancer, vitamin D, vitamin D receptor gene polymorphism of vitamin D, mastodynia, dishormonal disease of the breast.

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Preeti Tanaji Mane, Sangram Prakash Patil, Balaji Sopanrao Wakure, and Pravin Shridhar Wakte. "Breast cancer: understanding etiology, addressing molecular signaling pathways, identifying therapeutic targets and strategizing the treatment." International Journal of Research in Pharmaceutical Sciences 12, no. 3 (July 1, 2021): 1757–69. http://dx.doi.org/10.26452/ijrps.v12i3.4779.

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Breast cancer has messed the life of a greater number of women being the most common cancer affecting them worldwide. A number of risk factors contribute the breast malignancy, however, genetic drift is accountable the most. Depending on the cell origin, invasiveness and receptors involved, breast cancer is classified into various subtypes. The accurate diagnosis of breast cancer is important as it defines the prognosis and directs the type of treatment required. A number of major signaling pathways involved in breast tumorigenesis and its development include estrogen receptors (ERs), HER2, Wnt/β-catenin, Notch, Hedgehog (Hh), PI3K and mTOR pathway. Furthermore, certain enzymes like Cyclin dependent kinases and breast tumor kinases also play a vital role in cell cycle regulation and therefore, in the development of breast neoplasms. Recent studies have also enlightened the role of non-coding RNAs in breast cancer development. This review discusses various aspects of breast cancer such as its etiology, subtypes, various signaling pathways involved, targets projected by these pathways and the current treatment options based on a few of these targets. Also, the role of different genes, enzymes and non-coding RNAs related to breast tumorigenesis and development is discussed.

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Granadillo Rodríguez, Milaid, Ben Flath, and Linda Chelico. "The interesting relationship between APOBEC3 deoxycytidine deaminases and cancer: a long road ahead." Open Biology 10, no. 12 (December 2020): 200188. http://dx.doi.org/10.1098/rsob.200188.

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Cancer is considered a group of diseases characterized by uncontrolled growth and spread of abnormal cells and is propelled by somatic mutations. Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3) family of enzymes are endogenous sources of somatic mutations found in multiple human cancers. While these enzymes normally act as an intrinsic immune defence against viruses, they can also catalyse ‘off-target’ cytidine deamination in genomic single-stranded DNA intermediates. The deamination of cytosine forms uracil, which is promutagenic in DNA. Key factors to trigger the APOBEC ‘off-target’ activity are overexpression in a non-normal cell type, nuclear localization and replication stress. The resulting uracil-induced mutations contribute to genomic variation, which may result in neutral, beneficial or harmful consequences for the cancer. This review summarizes the functional and biochemical basis of the APOBEC3 enzyme activity and highlights their relationship with the most well-studied cancers in this particular context such as breast, lung, bladder, and human papillomavirus-associated cancers. We focus on APOBEC3A, APOBEC3B and APOBEC3H haplotype I because they are the leading candidates as sources of somatic mutations in these and other cancers. Also, we discuss the prognostic value of the APOBEC3 expression in drug resistance and response to therapies.

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Risha, Y., V. Susevski, N. Hüttmann, S. Poolsup, Z. Minic, and M. V. Berezovski. "Proteome of breast cancer derived microvesicles." Siberian Medical Review, no. 2 (2021): 68–71. http://dx.doi.org/10.20333/25000136-2021-2-68-71.

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The aim of the research. To examine the proteomic profi le of breast cancer exosomes. Material and methods. Cell lines used for this study were MDA-MB-231 female epithelial breast cancer cells (ATCC HTB-26) and MCF10A non-tumorigenic epithelial breast tissue cells. MVs were isolated using diff erential ultracentrifugation. Samples were lysed, reduced, alkylated, digested, and analyzed by an Orbitrap Fusion mass spectrometer. MS raw fi les were analyzed using MaxQuant version 1.6.12.0. Peptides were searched against the human UniProt FASTA database using the Andromeda search engine, integrated into MaxQuant. Results. MVs derived from MCF10A and MDA-MB-231 cell lines were analyzed, and 1427 and 547 proteins were identifi ed in the MDA-MB-231 and MCF10A-derived MVs, respectively. In total, 455 proteins were common to both MDA-MB-231 and MCF10A MVs. MVs derived from MCF10A and MDAMB-231 cell lines were analyzed, and 1427 and 547 proteins were identifi ed in the MDA-MB-231 and MCF10A-derived MVs, respectively. In total, 455 proteins were common to both MDA-MB-231 and MCF10A MVs. Th e unique MDA-MB-231 MV proteins were searched against the DisGeNET human diseases database. Out of 972 MDA-MB-231 MV proteins, 112 were cancer-related while 32 were specifi cally associated with BC. In the MDA-MB-231 MV proteome, 23 Wnt signaling pathway proteins were identifi ed based on their GO biological process. Proteomic analysis identifi ed enzymes OAT, TALDO1, and BLMH were only in MVs from metastatic MDA-MB-231 cell line. The specific activity of OAT and TALDO1 was higher in MV fractions of MDA-MB-231 in comparison to the non-cancerous MCF10A cell line-derived MVs. Th ese fi ndings might suggest that these enzymes might play a role in BC. In our present study, we found that some enzymes identifi ed from MV fractions were already proposed to play a role in cancer therapy as therapeutic targets (OAT, TALDO1) and resistance against chemotherapy agents (BLMH).

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Pippa, Simone, Cecilia Mannironi, Valerio Licursi, Luca Bombardi, Gianni Colotti, Enrico Cundari, Adriano Mollica, et al. "Small Molecule Inhibitors of KDM5 Histone Demethylases Increase the Radiosensitivity of Breast Cancer Cells Overexpressing JARID1B." Molecules 24, no. 9 (May 4, 2019): 1739. http://dx.doi.org/10.3390/molecules24091739.

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Background: KDM5 enzymes are H3K4 specific histone demethylases involved in transcriptional regulation and DNA repair. These proteins are overexpressed in different kinds of cancer, including breast, prostate and bladder carcinomas, with positive effects on cancer proliferation and chemoresistance. For these reasons, these enzymes are potential therapeutic targets. Methods: In the present study, we analyzed the effects of three different inhibitors of KDM5 enzymes in MCF-7 breast cancer cells over-expressing one of them, namely KDM5B/JARID1B. In particular we tested H3K4 demethylation (western blot); radio-sensitivity (cytoxicity and clonogenic assays) and damage accumulation (COMET assay and kinetics of H2AX phosphorylation). Results: we show that all three compounds with completely different chemical structures can selectively inhibit KDM5 enzymes and are capable of increasing sensitivity of breast cancer cells to ionizing radiation and radiation-induced damage. Conclusions: These findings confirm the involvement of H3K4 specific demethylases in the response to DNA damage, show a requirement of the catalytic function and suggest new strategies for the therapeutic use of their inhibitors.

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Kutryb-Zajac, Barbara, Gabriela Harasim, Agata Jedrzejewska, Oliwia Krol, Alicja Braczko, Patrycja Jablonska, Paulina Mierzejewska, Jacek Zielinski, Ewa M. Slominska, and Ryszard T. Smolenski. "Macrophage-Derived Adenosine Deaminase 2 Correlates with M2 Macrophage Phenotype in Triple Negative Breast Cancer." International Journal of Molecular Sciences 22, no. 7 (April 5, 2021): 3764. http://dx.doi.org/10.3390/ijms22073764.

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Several lines of evidence suggest that altered adenosine deaminase (ADA) activity, especially its ADA2 iso-enzyme, is associated with malignant breast cancer (BC) development. Triple-negative breast cancer (TNBC) is currently the most challenging BC subtype due to its metastatic potential and recurrence. Herein, we analyzed the sources of ADA iso-enzymes in TNBC by investigating the effects of cell-to-cell interactions between TNBC cells, macrophages, lymphocytes, and endothelial cells. We also examined the potential relationship between ADA activity and cancer progression in TNBC patients. In vitro analyses demonstrated that the interactions of immune and endothelial cells with MDA-MB-231 triple negative BC cells modulated their extracellular adenosine metabolism pattern. However, they caused an increase in the ADA1 activity, and did not alter ADA2 activity in cancer cells. In turn, the co-culture of MDA-MB-231 cells with THP-1 monocyte/macrophages, Jurkat cells, and human lung microvascular endothelial cells (HULEC) caused the increase in ADA2 activity on THP-1 cells and ADA1 activity on Jurkat cells and HULEC. Clinical sample analysis revealed that TNBC patients had higher plasma ADA2 activities and lower ADA1/ADA2 ratio at advanced stages of cancer development than in the initial stages, while patients with hormone receptor positive, HER2 negative (HR+HER2-), and triple positive (HR+HER2+) breast cancers at the same stages showed opposite trends. TNBC patients also demonstrated positive associations between plasma ADA2 activity and pro-tumor M2 macrophage markers, as well as between ADA1 activity and endothelial dysfunction or inflammatory parameters. The analysis of TNBC patients, at 6 and 12 months following cancer treatment, did not showed significant changes in plasma ADA activities and macrophage polarization markers, which may be the cause of their therapeutic failure. We conclude that alterations in both ADA iso-enzymes can play a role in breast cancer development and progression by the modulation of extracellular adenosine-dependent pathways. Additionally, the changes in ADA2 activity that may contribute to the differentiation of macrophages into unfavorable pro-tumor M2 phenotype deserve special attention in TNBC.

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Wang, Haiwei, Xinrui Wang, Liangpu Xu, Ji Zhang, and Hua Cao. "High expression levels of pyrimidine metabolic rate–limiting enzymes are adverse prognostic factors in lung adenocarcinoma: a study based on The Cancer Genome Atlas and Gene Expression Omnibus datasets." Purinergic Signalling 16, no. 3 (July 8, 2020): 347–66. http://dx.doi.org/10.1007/s11302-020-09711-4.

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Abstract Reprogramming of metabolism is described in many types of cancer and is associated with the clinical outcomes. However, the prognostic significance of pyrimidine metabolism signaling pathway in lung adenocarcinoma (LUAD) is unclear. Using the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) datasets, we found that the pyrimidine metabolism signaling pathway was significantly enriched in LUAD. Compared with normal lung tissues, the pyrimidine metabolic rate–limiting enzymes were highly expressed in lung tumor tissues. The high expression levels of pyrimidine metabolic–rate limiting enzymes were associated with unfavorable prognosis. However, purinergic receptors P2RX1, P2RX7, P2RY12, P2RY13, and P2RY14 were relatively downregulated in lung cancer tissues and were associated with favorable prognosis. Moreover, we found that hypo-DNA methylation, DNA amplification, and TP53 mutation were contributing to the high expression levels of pyrimidine metabolic rate–limiting enzymes in lung cancer cells. Furthermore, combined pyrimidine metabolic rate–limiting enzymes had significant prognostic effects in LUAD. Comprehensively, the pyrimidine metabolic rate–limiting enzymes were highly expressed in bladder cancer, breast cancer, colon cancer, liver cancer, and stomach cancer. And the high expression levels of pyrimidine metabolic rate–limiting enzymes were associated with unfavorable prognosis in liver cancer. Overall, our results suggested the mRNA levels of pyrimidine metabolic rate–limiting enzymes CAD, DTYMK, RRM1, RRM2, TK1, TYMS, UCK2, NR5C2, and TK2 were predictive of lung cancer as well as other cancers.

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41

Bajin-Katic, Katica. "Comparison of glycolytic enzyme and isoenzyme activity in breast cancers and dysplasia." Medical review 65, no. 5-6 (2012): 200–205. http://dx.doi.org/10.2298/mpns1206200b.

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The study was aimed at assessing the total enzyme activity and the profile of breast cancer and dysplasia on the human material. In addition, the validity of data was evaluated from the aspect of improving diagnostics. Lactate dehydrogenase activity, as well as the profile of its isoenzymes, pyruvate kinase and hexokinase, were measured. The study included 60 samples of breast cancer, out of which 20 were benign breast tumours and 40 were 1st and 2nd degree dysplasia of the breast. The samples were collected from the patients operated at the Institute for Oncology of Faculty of Medicine in Sremska Kamenica. Lactate dehydrogenase isoenzymes were separated by the vertical polyacrylamide gel disc electrophoresis according to the slightly modified Brewer and Ashworth?s method. The activity of all the tested enzymes was measured under the conditions of linear kinetics in the function of time and enzyme concentration. Lactate dehydrogenase-5 was found in 88% of the analyzed breast cancer samples, whereas it was not detected in breast dysplasia. Pyruvate kinase (4.-isoenzyme) was about 50 times higher and the activity of hexokinase was 3 times higher in breast cancer than in breast dysplasia. Lactate dehydrogenase-5 and pyruvate kinase (4.-isoenzyme) are particularly important and reliable markers of malignity. The results obtained for quantitative and qualitative changes in the enzyme activity can be used to improve diagnostics and early diagnostics of malignant breast neoplasm.

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42

Tian, Ye, Yicong Bian, Yan Jiang, Sainan Qian, Aiming Yu, and Su Zeng. "Interplay of Breast Cancer Resistance Protein (BCRP) and Metabolizing Enzymes." Current Drug Metabolism 16, no. 10 (December 10, 2015): 877–93. http://dx.doi.org/10.2174/138920021610151210184205.

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Mishra, Alok, Ashutosh Shrivastava, Anshuman Srivastava, and Sudhir Kumar Verma. "PROGNOSTIC SIGNIFICANCE OF DEIODINASE ENZYMES MRNA EXPRESSION IN BREAST CANCER." Journal of Evidence Based Medicine and Healthcare 6, no. 34 (August 26, 2019): 2343–46. http://dx.doi.org/10.18410/jebmh/2019/479.

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44

Pasqualini, Jorge R. "Breast cancer and steroid metabolizing enzymes: The role of progestogens." Maturitas 65 (December 2009): S17—S21. http://dx.doi.org/10.1016/j.maturitas.2009.11.006.

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45

Du, Jinlin, Brendan P. Keegan, and William G. North. "Key peptide processing enzymes are expressed by breast cancer cells." Cancer Letters 165, no. 2 (April 2001): 211–18. http://dx.doi.org/10.1016/s0304-3835(01)00409-8.

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46

Westermarck, T., M. Kantola, H. Mussalo-Rauhamaa, and F. Atroshi. "Trace elements and glutathione-enzymes in human breast cancer tissue." Free Radical Biology and Medicine 9 (January 1990): 176. http://dx.doi.org/10.1016/0891-5849(90)90798-n.

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Dowsett, M. "Inhibitors of steroidogenic enzymes for the treatment of breast cancer." Journal of Steroid Biochemistry and Molecular Biology 39, no. 5 (November 1991): 805–9. http://dx.doi.org/10.1016/0960-0760(91)90029-5.

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48

Kalezic, Andjelika, Mirjana Udicki, Biljana Srdic Galic, Marija Aleksic, Aleksandra Korac, Aleksandra Jankovic, and Bato Korac. "Tissue-Specific Warburg Effect in Breast Cancer and Cancer-Associated Adipose Tissue—Relationship between AMPK and Glycolysis." Cancers 13, no. 11 (May 31, 2021): 2731. http://dx.doi.org/10.3390/cancers13112731.

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Typical features of the breast malignant phenotype rely on metabolic reprogramming of cancer cells and their interaction with surrounding adipocytes. Obesity is strongly associated with breast cancer mortality, yet the effects of obesity on metabolic reprogramming of cancer and cancer-associated adipose tissue remain largely unknown. Paired biopsies of breast tumor tissue and adipose tissue from premenopausal women were divided according to pathohistological analyses and body mass index on normal-weight and overweight/obese with benign or malignant tumors. We investigated the protein expression of key regulatory enzymes of glycolysis, pentose phosphate pathway (PPP), and glycogen synthesis. Breast cancer tissue showed a simultaneous increase in 5′-AMP-activated protein kinase (AMPK) protein expression with typical features of the Warburg effect, including hexokinase 2 (HK 2) overexpression and its association with mitochondrial voltage-dependent anion-selective channel protein 1, associated with an overexpression of rate-limiting enzymes of glycolysis (phosphofructokinase 1—PFK-1) and pentose phosphate pathway (glucose-6-phosphate dehydrogenase—G6PDH). In parallel, cancer-associated adipose tissue showed increased AMPK protein expression with overexpression of HK 2 and G6PDH in line with increased PPP activity. Moreover, important obesity-associated differences in glucose metabolism were observed in breast cancer tissue showing prominent glycogen deposition and higher glycogen synthase kinase-3 protein expression in normal-weight women and higher PFK-1 and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) protein expression in overweight/obese women. In conclusion, metabolic reprogramming of glycolysis contributes to tissue-specific Warburg effect in breast cancer and cancer-associated adipose tissue.

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Niklaus, Nicolas J., Igor Tokarchuk, Mara Zbinden, Anna M. Schläfli, Paola Maycotte, and Mario P. Tschan. "The Multifaceted Functions of Autophagy in Breast Cancer Development and Treatment." Cells 10, no. 6 (June 9, 2021): 1447. http://dx.doi.org/10.3390/cells10061447.

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Macroautophagy (herein referred to as autophagy) is a complex catabolic process characterized by the formation of double-membrane vesicles called autophagosomes. During this process, autophagosomes engulf and deliver their intracellular content to lysosomes, where they are degraded by hydrolytic enzymes. Thereby, autophagy provides energy and building blocks to maintain cellular homeostasis and represents a dynamic recycling mechanism. Importantly, the clearance of damaged organelles and aggregated molecules by autophagy in normal cells contributes to cancer prevention. Therefore, the dysfunction of autophagy has a major impact on the cell fate and can contribute to tumorigenesis. Breast cancer is the most common cancer in women and has the highest mortality rate among all cancers in women worldwide. Breast cancer patients often have a good short-term prognosis, but long-term survivors often experience aggressive recurrence. This phenomenon might be explained by the high heterogeneity of breast cancer tumors rendering mammary tumors difficult to target. This review focuses on the mechanisms of autophagy during breast carcinogenesis and sheds light on the role of autophagy in the traits of aggressive breast cancer cells such as migration, invasion, and therapeutic resistance.

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Avtandilyan, Nikolay, Hayarpi Javrushyan, Gayane Petrosyan, and Armen Trchounian. "The Involvement of Arginase and Nitric Oxide Synthase in Breast Cancer Development: Arginase and NO Synthase as Therapeutic Targets in Cancer." BioMed Research International 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/8696923.

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It is well established that, during development of malignancies, metabolic changes occur, including alterations of enzyme activities and isoenzyme expression. Arginase and nitric oxide (NO) synthase (NOS) are two of those enzymes considered to be involved in tumorigenesis. The goal of this article was to study the involvement of arginase and NOS in the development of different stages of breast cancer. Our results have shown that human serum arginase activity and NO (resp., and NOS activity) and polyamines quantities increased in parallel with cancer stage progression and decreased after neoadjuvant chemotherapy. For breast cancer, the only isoenzyme of arginase expressed in serum before and after chemotherapy was in a cationic form. The data of Lineweaver-Burk plot with aKmvalue of 2 mM was calculated, which is characteristic for human liver type isoform of arginase. During electrophoresis at pH 8.9, the enzyme exhibited high electrophoretic mobility and was detected near the anode. The presented results demonstrated that arginase in human serum with breast cancer and after chemotherapy is not polymorphic. We suggest that arginase and NOS inhibition has antitumor effects on cancer development, as it can inhibit polyamines and NO levels, a precursor of cancer cell proliferation, metastasis, and tumor angiogenesis.

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Journal articles on the topic 'Enzymes; Breast cancer'

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