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Journal articles on the topic 'BREAST PROGRESSION'

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Author: Grafiati

Published: 11 March 2023

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1

Arafat, Kholoud, Elham Al Kubaisy, Shahrazad Sulaiman, Sherif M. Karam, Zeina Al Natour, Ahmed H. Hassan, and Samir Attoub. "SMARCAD1 in Breast Cancer Progression." Cellular Physiology and Biochemistry 50, no. 2 (2018): 489–500. http://dx.doi.org/10.1159/000494163.

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Background/Aims: Breast cancer is the most common cancer in women worldwide, and within this cancer type, triple-negative breast cancers have the worst prognosis. The identification of new genes associated with triple-negative breast cancer progression is crucial for developing more specific anti-cancer targeted therapies, which could lead to a better management of these patients. In this context, we have recently demonstrated that SMARCAD1, a DEAD/H box-containing helicase, is involved in breast cancer cell migration, invasion, and metastasis. The aim of this study was to investigate the impact of the stable knockdown of SMARCAD1 on human breast cancer cell progression. Methods: Using two different designs of shRNA targeting SMARCAD1, we investigated the impact of the stable knockdown of SMARCAD1 on human breast cancer cell proliferation and colony growth in vitro and on tumour growth in chick embryo and nude mouse xenograft models in vivo using MDA-MB-231 (ER-/PR-/ HER2-) and T47D (ER+/PR+/-/HER2-) human breast cancer cell lines. Results: We found that SMARCAD1 knockdown resulted in a significant decrease in breast cancer cell proliferation and colony formation, leading to the significant inhibition of tumour growth in both the chick embryo and nude mouse xenograft models. This inhibition was due, at least in part, to a decrease in IKKβ expression. Conclusion: These results indicate that SMARCAD1 is involved in breast cancer progression and can be a promising target for breast cancer therapy.

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2

Gespach, Christian. "Reciprocity in breast cancer progression." Oncotarget 5, no. 22 (November 30, 2014): 10967–68. http://dx.doi.org/10.18632/oncotarget.2853.

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Chen, Yinghua, and Olufunmilayo I. Olopade. "MYC in breast tumor progression." Expert Review of Anticancer Therapy 8, no. 10 (October 2008): 1689–98. http://dx.doi.org/10.1586/14737140.8.10.1689.

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4

Dalgin, Gul S., Gabriela Alexe, Daniel Scanfeld, Pablo Tamayo, Jill P. Mesirov, Shridar Ganesan, Charles DeLisi, and Gyan Bhanot. "Portraits of breast cancer progression." BMC Bioinformatics 8, no. 1 (2007): 291. http://dx.doi.org/10.1186/1471-2105-8-291.

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5

Ma, L. "Determinants of Breast Cancer Progression." Science Translational Medicine 6, no. 243 (July 2, 2014): 243fs25. http://dx.doi.org/10.1126/scitranslmed.3009587.

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6

SUBRAMANIAN, BALAKRISHNA, and DAVID E. AXELROD. "Progression of Heterogeneous Breast Tumors." Journal of Theoretical Biology 210, no. 1 (May 2001): 107–19. http://dx.doi.org/10.1006/jtbi.2001.2302.

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7

Kontomanolis, Emmanuel N., Sofia Kalagasidou, Stamatia Pouliliou, Xanthoula Anthoulaki, Nikolaos Georgiou, Valentinos Papamanolis, and Zacharias N. Fasoulakis. "The Notch Pathway in Breast Cancer Progression." Scientific World Journal 2018 (July 8, 2018): 1–11. http://dx.doi.org/10.1155/2018/2415489.

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Objective. Notch signaling pathway is a vital parameter of the mammalian vascular system. In this review, the authors summarize the current knowledge about the impact of the Notch signaling pathway in breast cancer progression and the therapeutic role of Notch’s inhibition.Methods. The available literature in MEDLINE, PubMed, and Scopus, regarding the role of the Notch pathway in breast cancer progression was searched for related articles from about 1973 to 2017 including terms such as “Notch,” “Breast Cancer,” and “Angiogenesis.”Results. Notch signaling controls the differentiation of breast epithelial cells during normal development. Studies confirm that the Notch pathway has a major participation in breast cancer progression through overexpression and/or abnormal genetic type expression of the notch receptors and ligands that determine angiogenesis. The cross-talk of Notch and estrogens, the effect of Notch in breast cancer stem cells formation, and the dependable Notch overexpression during breast tumorigenesis have been studied enough and undoubtedly linked to breast cancer development. The already applied therapeutic inhibition of Notch for breast cancer can drastically change the course of the disease.Conclusion. Current data prove that Notch pathway has a major participation and multiple roles during breast tumor progression. Inhibition of Notch receptors and ligands provides innovative therapeutic results and could become the therapy of choice in the next few years, even though further research is needed to reach safe conclusions.

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Ferreira, Sandra, Nuno Saraiva, Patrícia Rijo, and Ana S. Fernandes. "LOXL2 Inhibitors and Breast Cancer Progression." Antioxidants 10, no. 2 (February 19, 2021): 312. http://dx.doi.org/10.3390/antiox10020312.

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LOX (lysyl oxidase) and lysyl oxidase like-1–4 (LOXL 1–4) are amine oxidases, which catalyze cross-linking reactions of elastin and collagen in the connective tissue. These amine oxidases also allow the cross-link of collagen and elastin in the extracellular matrix of tumors, facilitating the process of cell migration and the formation of metastases. LOXL2 is of particular interest in cancer biology as it is highly expressed in some tumors. This protein also promotes oncogenic transformation and affects the proliferation of breast cancer cells. LOX and LOXL2 inhibition have thus been suggested as a promising strategy to prevent metastasis and invasion of breast cancer. BAPN (β-aminopropionitrile) was the first compound described as a LOX inhibitor and was obtained from a natural source. However, novel synthetic compounds that act as LOX/LOXL2 selective inhibitors or as dual LOX/LOX-L inhibitors have been recently developed. In this review, we describe LOX enzymes and their role in promoting cancer development and metastases, with a special focus on LOXL2 and breast cancer progression. Moreover, the recent advances in the development of LOXL2 inhibitors are also addressed. Overall, this work contextualizes and explores the importance of LOXL2 inhibition as a promising novel complementary and effective therapeutic approach for breast cancer treatment.

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9

Skinner, Kristin A., C. Alan Kachel, Raymond Sullivan, Andrew Jones, and Soudamini Kurumboor. "Progressive accumulation of DNA methylation with malignant progression in breast tissue." Journal of the American College of Surgeons 199, no. 3 (September 2004): 85. http://dx.doi.org/10.1016/j.jamcollsurg.2004.05.184.

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10

Artacho-Cordón, Antonia, Francisco Artacho-Cordón, Sandra Ríos-Arrabal, Irene Calvente, and María Isabel Núñez. "Tumor microenvironment and breast cancer progression." Cancer Biology & Therapy 13, no. 1 (January 2012): 14–24. http://dx.doi.org/10.4161/cbt.13.1.18869.

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11

Herr, Ingrid, and Alexander Marmé. "Glucocorticoids and progression of breast cancer." Cancer Biology & Therapy 4, no. 12 (December 2005): 1415–16. http://dx.doi.org/10.4161/cbt.4.12.2354.

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12

Kufel-Grabowska, Joanna, Iwona Mozer-Lisewska, Witold Cholewiński, Mikołaj Bartoszkiewicz, and Maria Litwiniuk. "Covid-19 mimicking breast cancer progression." Palliative Medicine 13, no. 2 (2021): 90–92. http://dx.doi.org/10.5114/pm.2021.106453.

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13

Гадецкая, Нина. "LEWIS C IN BREAST CANCER PROGRESSION." Hematology, Transfusion and Cell Therapy 43 (November 2021): S20—S21. http://dx.doi.org/10.1016/j.htct.2021.10.981.

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14

Todorović-Raković, Nataša, and Jelena Milovanović. "Interleukin-8 in Breast Cancer Progression." Journal of Interferon & Cytokine Research 33, no. 10 (October 2013): 563–70. http://dx.doi.org/10.1089/jir.2013.0023.

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15

&NA;. "Trastuzumab safe in breast cancer progression?" Reactions Weekly &NA;, no. 1005 (June 2004): 4. http://dx.doi.org/10.2165/00128415-200410050-00009.

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16

Yang, J., D. R. Bielenberg, S. J. Rodig, R. Doiron, M. C. Clifton, A. L. Kung, R. K. Strong, D. Zurakowski, and M. A. Moses. "Lipocalin 2 promotes breast cancer progression." Proceedings of the National Academy of Sciences 106, no. 10 (February 23, 2009): 3913–18. http://dx.doi.org/10.1073/pnas.0810617106.

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17

Couch, Fergus, Youzhen Wang, Kathleen Steinmann, YongYao Xu, Maureen Mertens, James Ingle, James Lillie, and Patrick Roche. "Expression analysis of breast cancer progression." Nature Genetics 27, S4 (April 2001): 49. http://dx.doi.org/10.1038/87048.

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18

Thiery, Jean Paul, and Matthew Morgan. "Breast cancer progression with a Twist." Nature Medicine 10, no. 8 (August 2004): 777–78. http://dx.doi.org/10.1038/nm0804-777.

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19

Kannan, Anbarasu, Robert B. Wells, Subramaniam Sivakumar, Satoshi Komatsu, Karan P. Singh, Buka Samten, Julie V. Philley, et al. "Mitochondrial Reprogramming Regulates Breast Cancer Progression." Clinical Cancer Research 22, no. 13 (February 17, 2016): 3348–60. http://dx.doi.org/10.1158/1078-0432.ccr-15-2456.

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20

Baker, Holly. "Breast cancer progression slowed by entinostat." Lancet Oncology 14, no. 8 (July 2013): e298. http://dx.doi.org/10.1016/s1470-2045(13)70286-9.

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21

Dirix, Luc Y., and Andrew R. Reynolds. "Bevacizumab beyond progression in breast cancer." Lancet Oncology 15, no. 11 (October 2014): 1190–91. http://dx.doi.org/10.1016/s1470-2045(14)70454-1.

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22

Andritsch, E., C. Farkas, S. Stanzer, T. Bauernhofer, and M. Vigier. "Psychoneuroimmunological predictors of breast cancer progression." Journal of Psychosomatic Research 133 (June 2020): 110081. http://dx.doi.org/10.1016/j.jpsychores.2020.110081.

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23

Schmidt, Emmett V. "Genes Involved in Breast Cancer Progression." American Journal of Pathology 161, no. 6 (December 2002): 1973–77. http://dx.doi.org/10.1016/s0002-9440(10)64473-2.

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24

Harrison, D. A., S. W. Duffy, E. Sala, R. M. L. Warren, E. Couto, and N. E. Day. "Deterministic models for breast cancer progression:." Journal of Clinical Epidemiology 55, no. 11 (November 2002): 1113–18. http://dx.doi.org/10.1016/s0895-4356(02)00483-3.

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25

Chakrabarti, Anirikh, Scott Verbridge, Abraham D. Stroock, Claudia Fischbach, and Jeffrey D. Varner. "Multiscale Models of Breast Cancer Progression." Annals of Biomedical Engineering 40, no. 11 (September 25, 2012): 2488–500. http://dx.doi.org/10.1007/s10439-012-0655-8.

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26

Yin, Wesley, Ruslan Horblyuk, Julia Jane Perkins, Steve Sison, Gregory Smith, Julia Thornton Snider, Yanyu Wu, and Tomas J. Philipson. "Breast cancer progression and workplace productivity." Journal of Clinical Oncology 33, no. 15_suppl (May 20, 2015): 6586. http://dx.doi.org/10.1200/jco.2015.33.15_suppl.6586.

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27

Gil Del Alcazar, Carlos R., Maša Alečković, and Kornelia Polyak. "Immune Escape during Breast Tumor Progression." Cancer Immunology Research 8, no. 4 (April 2020): 422–27. http://dx.doi.org/10.1158/2326-6066.cir-19-0786.

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28

Polyak, K. "Is Breast Tumor Progression Really Linear?" Clinical Cancer Research 14, no. 2 (January 15, 2008): 339–41. http://dx.doi.org/10.1158/1078-0432.ccr-07-2188.

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29

Ingvarsson, Sigurdur. "Molecular genetics of breast cancer progression." Seminars in Cancer Biology 9, no. 4 (August 1999): 277–88. http://dx.doi.org/10.1006/scbi.1999.0124.

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30

Christgen, Matthias, Monika Noskowicz, Elisa Schipper, Henriette Christgen, Charlotte Heil, Till Krech, Florian Länger, Hans Kreipe, and Ulrich Lehmann. "OncogenicPIK3CAmutations in lobular breast cancer progression." Genes, Chromosomes and Cancer 52, no. 1 (September 21, 2012): 69–80. http://dx.doi.org/10.1002/gcc.22007.

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31

Dairkee, Shanaz H., and Helene S. Smith. "Genetic analysis of breast cancer progression." Journal of Mammary Gland Biology and Neoplasia 1, no. 2 (April 1996): 139–51. http://dx.doi.org/10.1007/bf02013638.

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32

Wang, Xuan, Christopher Qian, Yinlong Yang, Meng-Yue Liu, Ya Ke, and Zhong-Ming Qian. "Phosphorylated Rasal2 facilitates breast cancer progression." EBioMedicine 50 (December 2019): 144–55. http://dx.doi.org/10.1016/j.ebiom.2019.11.019.

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33

Tower, Ruppert, and Britt. "The Immune Microenvironment of Breast Cancer Progression." Cancers 11, no. 9 (September 16, 2019): 1375. http://dx.doi.org/10.3390/cancers11091375.

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Inflammation is now recognized as a hallmark of cancer. Genetic changes in the cancer cell are accepted as the match that lights the fire, whilst inflammation is seen as the fuel that feeds the fire. Once inside the tumour, the immune cells secrete cytokines that kick-start angiogenesis to ferry in much-needed oxygen and nutrients that encourage the growth of tumours. There is now irrefutable data demonstrating that the immune contexture of breast tumours can influence growth and metastasis. A higher immune cell count in invasive breast cancer predicts prognosis and response to chemotherapy. We are beginning now to define the specific innate and adaptive immune cells present in breast cancer and their role not just in the progression of invasive disease, but also in the development of pre-invasive lesions and their transition to malignant tumours. This review article focusses on the immune cells present in early stage breast cancer and their relationship with the immunoediting process involved in tumour advancement.

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34

Górnicki, Tomasz, Jakub Lambrinow, Monika Mrozowska, Hanna Romanowicz, Beata Smolarz, Aleksandra Piotrowska, Agnieszka Gomułkiewicz, Marzena Podhorska-Okołów, Piotr Dzięgiel, and Jędrzej Grzegrzółka. "Expression of RBMS3 in Breast Cancer Progression." International Journal of Molecular Sciences 24, no. 3 (February 2, 2023): 2866. http://dx.doi.org/10.3390/ijms24032866.

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The aim of the study was to evaluate the localization and intensity of RNA-binding motif single-stranded-interacting protein 3 (RBMS3) expression in clinical material using immunohistochemical (IHC) reactions in cases of ductal breast cancer (in vivo), and to determine the level of RBMS3 expression at both the protein and mRNA levels in breast cancer cell lines (in vitro). Moreover, the data obtained in the in vivo and in vitro studies were correlated with the clinicopathological profiles of the patients. Material for the IHC studies comprised 490 invasive ductal carcinoma (IDC) cases and 26 mastopathy tissues. Western blot and RT-qPCR were performed on four breast cancer cell lines (MCF-7, BT-474, SK-BR-3 and MDA-MB-231) and the HME1-hTERT (Me16C) normal immortalized breast epithelial cell line (control). The Kaplan–Meier plotter tool was employed to analyze the predictive value of overall survival of RBMS3 expression at the mRNA level. Cytoplasmatic RBMS3 IHC expression was observed in breast cancer cells and stromal cells. The statistical analysis revealed a significantly decreased RBMS3 expression in the cancer specimens when compared with the mastopathy tissues (p < 0.001). An increased expression of RBMS3 was corelated with HER2(+) cancer specimens (p < 0.05) and ER(−) cancer specimens (p < 0.05). In addition, a statistically significant higher expression of RBMS3 was observed in cancer stromal cells in comparison to the control and cancer cells (p < 0.0001). The statistical analysis demonstrated a significantly higher expression of RBMS3 mRNA in the SK-BR-3 cell line compared with all other cell lines (p < 0.05). A positive correlation was revealed between the expression of RBMS3, at both the mRNA and protein levels, and longer overall survival. The differences in the expression of RBMS3 in cancer cells (both in vivo and in vitro) and the stroma of breast cancer with regard to the molecular status of the tumor may indicate that RBMS3 could be a potential novel target for the development of personalized methods of treatment. RBMS3 can be an indicator of longer overall survival for potential use in breast cancer diagnostic process.

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35

Murphy, L. C., and P. Watson. "Steroid receptors in human breast tumorigenesis and breast cancer progression." Biomedicine & Pharmacotherapy 56, no. 2 (March 2002): 65–77. http://dx.doi.org/10.1016/s0753-3322(01)00157-3.

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36

Kaur, Dr Sukhleen, Dr Kanwardeep Kaur, Dr Vijay Kumar Bodal, and Dr Jasmine Kaur. "Primary Squamous Cell Carcinoma of the Breast with Metastasis-A Rare Case Report." Scholars Journal of Applied Medical Sciences 11, no. 1 (January 5, 2022): 7–10. http://dx.doi.org/10.36347/sjams.2023.v11i01.002.

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Primary squamous cell carcinoma of breast is extremely rare invasive breast carcinoma with rapid progression with incidence of 0.1% and worse prognosis. Careful assessment and diagnosis of the entity should be considered in a rapidly progressing breast tumor. We hereby reported a case of primary carcinoma breast in 80-year-old female who was managed at tertiary care centre of Rajindra Hospital, Patiala.

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37

Zhong, Xiaorong, Ting Luo, Ling Deng, Pei Liu, Kejia Hu, Donghao Lu, Dan Zheng, et al. "Multidimensional Machine Learning Personalized Prognostic Model in an Early Invasive Breast Cancer Population-Based Cohort in China: Algorithm Validation Study." JMIR Medical Informatics 8, no. 11 (November 9, 2020): e19069. http://dx.doi.org/10.2196/19069.

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Background Current online prognostic prediction models for breast cancer, such as Adjuvant! Online and PREDICT, are based on specific populations. They have been well validated and widely used in the United States and Western Europe; however, several validation attempts in non-European countries have revealed suboptimal predictions. Objective We aimed to develop an advanced breast cancer prognosis model for disease progression, cancer-specific mortality, and all-cause mortality by integrating tumor, demographic, and treatment characteristics from a large breast cancer cohort in China. Methods This study was approved by the Clinical Test and Biomedical Ethics Committee of West China Hospital, Sichuan University on May 17, 2012. Data collection for this project was started in May 2017 and ended in March 2019. Data on 5293 women diagnosed with stage I to III invasive breast cancer between 2000 and 2013 were collected. Disease progression, cancer-specific mortality, all-cause mortality, and the likelihood of disease progression or death within a 5-year period were predicted. Extreme gradient boosting was used to develop the prediction model. Model performance was assessed by calculating the area under the receiver operating characteristic curve (AUROC), and the model was calibrated and compared with PREDICT. Results The training, test, and validation sets comprised 3276 (499 progressions, 202 breast cancer-specific deaths, and 261 all-cause deaths within 5-year follow-up), 1405 (211 progressions, 94 breast cancer-specific deaths, and 129 all-cause deaths), and 612 (109 progressions, 33 breast cancer-specific deaths, and 37 all-cause deaths) women, respectively. The AUROC values for disease progression, cancer-specific mortality, and all-cause mortality were 0.76, 0.88, and 0.82 for training set; 0.79, 0.80, and 0.83 for the test set; and 0.79, 0.84, and 0.88 for the validation set, respectively. Calibration analysis demonstrated good agreement between predicted and observed events within 5 years. Comparable AUROC and calibration results were confirmed in different age, residence status, and receptor status subgroups. Compared with PREDICT, our model showed similar AUROC and improved calibration values. Conclusions Our prognostic model exhibits high discrimination and good calibration. It may facilitate prognosis prediction and clinical decision making for patients with breast cancer in China.

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38

Tiainen, Satu, Amro Masarwah, Sanna Oikari, Kirsi Rilla, Kirsi Hämäläinen, Mazen Sudah, Anna Sutela, et al. "Tumor microenvironment and breast cancer survival: combined effects of breast fat, M2 macrophages and hyaluronan create a dismal prognosis." Breast Cancer Research and Treatment 179, no. 3 (November 12, 2019): 565–75. http://dx.doi.org/10.1007/s10549-019-05491-7.

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Abstract Purpose Tumor microenvironment, including inflammatory cells, adipocytes and extracellular matrix constituents such as hyaluronan (HA), impacts on cancer progression. Systemic metabolism also influences tumor growth e.g. obesity and type 2 diabetes (T2D) are risk factors for breast cancer. Here, in 262 breast cancer cases, we explored the combined impacts on survival of M2-like tumor associated macrophages (TAMs), the abundance of breast fat visualized as low density in mammograms, and tumor HA, and their associations with T2D. Methods Mammographic densities were assessed visually from the diagnostic images and dichotomized into very low density (VLD, density ≤ 10%, “fatty breast”) and mixed density (MID, density > 10%). The amounts of TAMs (CD163+ and CD68+) and tumor HA were determined by immunohistochemistry. The data of T2D was collected from the patient records. Statistical differences between the parameters were calculated with Chi square or Mann–Whitney test and survival analyses with Cox’s model. Results A combination of fatty breasts (VLD), abundance of M2-like TAMs (CD163+) and tumor HA associated with poor survival, as survival was 88–89% in the absence of these factors but only 40–47% when all three factors were present (p < 0.001). Also, an association between T2D and fatty breasts was found (p < 0.01). Furthermore, tumors in fatty breasts contained more frequently high levels of M2-like TAMs than tumors in MID breasts (p = 0.01). Conclusions Our results demonstrate a dramatic effect of the tumor microenvironment on breast cancer progression. We hypothesize that T2D as well as obesity increase the fat content of the breasts, subsequently enhancing local pro-tumoral inflammation.

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Fribbens, Charlotte Victoria, Isaac Garcia-Murillas, Matthew Beaney, Sarah Hrebien, Karen Howarth, Michael Epstein, Nitzan Rosenfeld, Alistair E. Ring, Stephen R. D. Johnston, and Nicholas C. Turner. "Tracking evolution of aromatase inhibitor resistance with circulating tumour DNA (ctDNA) in metastatic breast cancer." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): 1015. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.1015.

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1015 Background: Selection of resistance mutations may play a major role in the development of endocrine resistance. ESR1 mutations are rare in primary breast cancer but have a high prevalence in patients treated with aromatase inhibitors (AI) for advanced breast cancer. We investigated the evolution of genetic resistance to first line AI therapy using sequential ctDNA sampling in patients with advanced breast cancer. Methods: Seventy-one patients on first line AI therapy for metastatic breast cancer were enrolled in a prospective study to collect plasma samples for ctDNA analysis every three months on therapy, and at disease progression. All plasma samples were analysed with ESR1 multiplex digital PCR assays, and samples at disease progression were analysed by InVision (enhanced tagged-amplicon sequencing). Mutations were tracked back through samples prior to disease progression to study the evolution of mutations on therapy. Results: Of the 34 patients who progressed on first line AI, 53% (18/34) had ESR1 mutations detectable at progression. Sequencing of progression plasma ctDNA identified polyclonal RAS mutations in 10.7% (3/28) progressing patients (2 polyclonal KRAS, 1 monoclonal HRAS), all of whom also had ESR1 mutations, and a patient with an activating p.R248C FGFR3 mutation. ESR1 mutations were subclonal in 78.6% (11/14) patients, with all RAS mutations being rare subclones. In serial tracking prior to progression, ESR1 mutations were detectable in plasma with a median of 5.3 months (95% CI 2.9-NA) prior to clinical progression. Conclusions: ESR1 mutations are found at high frequency in patients progressing on AI, but are frequently sub-clonal and may not be the sole driver of AI resistance in these patients. Poly-clonal KRAS mutations are identified as a novel mechanism of resistance to AI, associated with detection of ESR1 mutations.

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40

Chen, Huijin, Yuanyuan Zhang, Xin Cao, and Peipei Mou. "MiR-27a Facilitates Breast Cancer Progression via GSK-3β." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382096557. http://dx.doi.org/10.1177/1533033820965576.

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Breast cancer remains one of the leading causes of cancer-associated death in women. MiR-27a is highly expressed in breast cancer tissue. However, the underlying mechanisms that promote breast cancer progression are unknown. In this study, we investigated the regulatory mechanisms of miR-27a and its target glycogen Synthase Kinase 3-β (GSK-3β) in breast cancer cells. We found that miR-27a was highly expressed in breast cancer tissues, which downregulated GSK-3β expression. We further identified GSK-3β as a direct target of miR-27a, and found that the miR-27a mediated suppression of GSK-3β activated Wnt/β-catenin-associated proliferative and invasive factor in breast cancer. The cell transfection assay demonstrated the overexpression of miR-27a also enhanced cell proliferation and invasion, and reduced cell apoptosis through GSK-3β. Finally, we demonstrated that the overexpression of miR-27a facilitated breast cancer progression through its ability to down-regulate the phosphorylation of GSK-3β both in vivo and vitro. These findings highlighted miR-27a as a novel therapeutic target in breast cancer.

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41

Li, Juan, Dominique Davidson, Cleiton Martins Souza, Ming-Chao Zhong, Ning Wu, Morag Park, William J. Muller, and André Veillette. "Loss of PTPN12 Stimulates Progression of ErbB2-Dependent Breast Cancer by Enhancing Cell Survival, Migration, and Epithelial-to-Mesenchymal Transition." Molecular and Cellular Biology 35, no. 23 (September 21, 2015): 4069–82. http://dx.doi.org/10.1128/mcb.00741-15.

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PTPN12 is a cytoplasmic protein tyrosine phosphatase (PTP) reported to be a tumor suppressor in breast cancer, through its capacity to dephosphorylate oncogenic receptor protein tyrosine kinases (PTKs), such as ErbB2. However, the precise molecular and cellular impact of PTPN12 deficiency in breast cancer progression remains to be fully clarified. Here, we addressed this issue by examining the effect of PTPN12 deficiency on breast cancer progressionin vivo, in a mouse model of ErbB2-dependent breast cancer using a conditional PTPN12-deficient mouse. Our studies showed that lack of PTPN12 in breast epithelial cells accelerated breast cancer development and lung metastasesin vivo. PTPN12-deficient breast cancer cells displayed enhanced tyrosine phosphorylation of the adaptor Cas, the adaptor paxillin, and the kinase Pyk2. They exhibited no detectable increase in ErbB2 tyrosine phosphorylation. PTPN12-deficient cells were more resistant to anoikis and had augmented migratory and invasive properties. Enhanced migration was corrected by inhibiting Pyk2. PTPN12-deficient breast cancer cells also acquired partial features of epithelial-to-mesenchymal transition (EMT), a feature of more aggressive forms of breast cancer. Hence, loss of PTPN12 promoted tumor progression in a mouse model of breast cancer, supporting the notion that PTPN12 is a tumor suppressor in human breast cancer. This function was related to the ability of PTPN12 to suppress cell survival, migration, invasiveness, and EMT and to inhibit tyrosine phosphorylation of Cas, Pyk2, and paxillin. These findings enhance our understanding of the role and mechanism of action of PTPN12 in the control of breast cancer progression.

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42

Vivacqua, Adele. "GPER1 and microRNA: Two Players in Breast Cancer Progression." International Journal of Molecular Sciences 22, no. 1 (December 24, 2020): 98. http://dx.doi.org/10.3390/ijms22010098.

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Breast cancer is the main cause of morbidity and mortality in women worldwide. However, the molecular pathogenesis of breast cancer remains poorly defined due to its heterogeneity. Several studies have reported that G Protein-Coupled Estrogen Receptor 1 (GPER1) plays a crucial role in breast cancer progression, by binding to estrogens or synthetic agonists, like G-1, thus modulating genes involved in diverse biological events, such as cell proliferation, migration, apoptosis, and metastasis. In addition, it has been established that the dysregulation of short sequences of non-coding RNA, named microRNAs (miRNAs), is involved in various pathophysiological conditions, including breast cancer. Recent evidence has indicated that estrogens may regulate miRNA expression and therefore modulate the levels of their target genes, not only through the classical estrogen receptors (ERs), but also activating GPER1 signalling, hence suggesting an alternative molecular pathway involved in breast tumor progression. Here, the current knowledge about GPER1 and miRNA action in breast cancer is recapitulated, reporting recent evidence on the liaison of these two players in triggering breast tumorogenic effects. Elucidating the role of GPER1 and miRNAs in breast cancer might provide new tools for innovative approaches in anti-cancer therapy.

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Sun, Aiqin, Xianyan Tian, Wannian Yang, and Qiong Lin. "Overexpression of SCYL1 Is Associated with Progression of Breast Cancer." Current Oncology 29, no. 10 (September 24, 2022): 6922–32. http://dx.doi.org/10.3390/curroncol29100544.

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SCYL1 is a pseudokinase and plays roles in cell division and gene transcription, nuclear/cytoplasmic shuttling of tRNA, protein glycosylation, and Golgi morphology. However, the role of SCYL1 in human breast cancer progression remains largely unknown. In this study, we determined expression of SCYL1 in breast cancer by searching the Cancer Genome Atlas (TCGA) and Tumor Immunoassay Resource (TIMER) databases. Meanwhile, we collected breast tumor tissue samples from 247 cases and detected expression of SCYL1 in the tumors using the tissue microarray assay (TMA). Association of SCYL1 with prognosis of breast cancer was determined based on the PrognoScan database. The results have shown that SCYL1 is overexpressed in breast cancer, and the expression of SCYL1 is associated with poor clinical outcomes of breast cancer patients. Furthermore, knockdown of SCYL1 by shRNAs significantly inhibited the proliferation and migration of breast cancer cells. Taken together, our data suggest that SCYL1 is a biomarker for poor prognosis of breast cancer, has a promoting role in breast cancer progression, and is a potential target for breast cancer therapy.

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Chen, Wenwen, Zhongyu Li, Pengwei Deng, Zhengnan Li, Yuhai Xu, Hongjing Li, Wentao Su, and Jianhua Qin. "Advances of Exosomal miRNAs in Breast Cancer Progression and Diagnosis." Diagnostics 11, no. 11 (November 20, 2021): 2151. http://dx.doi.org/10.3390/diagnostics11112151.

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Breast cancer is one of the most commonly diagnosed malignancies and the leading cause of cancer death in women worldwide. Although many factors associated with breast cancer have been identified, the definite etiology of breast cancer is still unclear. In addition, early diagnosis of breast cancer remains challenging. Exosomes are membrane-bound nanovesicles secreted by most types of cells and contain a series of biologically important molecules, such as lipids, proteins, and miRNAs, etc. Emerging evidence shows that exosomes can affect the status of cells by transmitting substances and messages among cells and are involved in various physiological and pathological processes. In breast cancer, exosomes play a significant role in breast tumorigenesis and progression through transfer miRNAs which can be potential biomarkers for early diagnosis of breast cancer. This review discusses the potential utility of exosomal miRNAs in breast cancer progression such as tumorigenesis, metastasis, immune regulation and drug resistance, and further in breast cancer diagnosis.

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Choi, Jinhyuk, Dong-Il Kim, Jinkyoung Kim, Baek-Hui Kim, and Aeree Kim. "Hornerin Is Involved in Breast Cancer Progression." Journal of Breast Cancer 19, no. 2 (2016): 142. http://dx.doi.org/10.4048/jbc.2016.19.2.142.

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Puleo, Julieann, and Kornelia Polyak. "The MCF10 Model of Breast Tumor Progression." Cancer Research 81, no. 16 (August 15, 2021): 4183–85. http://dx.doi.org/10.1158/0008-5472.can-21-1939.

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Hahm, Bong-Jin, Booil Jo, Firdaus S. Dhabhar, Oxana Palesh, Arianna Aldridge-Gerry, Sepideh N. Bajestan, Eric Neri, Bita Nouriani, David Spiegel, and Jamie M. Zeitzer. "Bedtime misalignment and progression of breast cancer." Chronobiology International 31, no. 2 (October 24, 2013): 214–21. http://dx.doi.org/10.3109/07420528.2013.842575.

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Seewaldt, Victoria L., and Victoria Scott. "Rapid Progression of Basal-Type Breast Cancer." New England Journal of Medicine 356, no. 13 (March 29, 2007): e12. http://dx.doi.org/10.1056/nejmicm063760.

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Gantov, Mariana, Priscila Pagnotta, Cecilia Lotufo, Gustavo Rindone, Maria Riera, Juan Calvo, and Judith Toneatto. "Beige adipocytes contribute to breast cancer progression." Oncology Reports 45, no. 1 (October 27, 2020): 317–28. http://dx.doi.org/10.3892/or.2020.7826.

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Newburger, D. E., D. Kashef-Haghighi, Z. Weng, R. Salari, R. T. Sweeney, A. L. Brunner, S. X. Zhu, et al. "Genome evolution during progression to breast cancer." Genome Research 23, no. 7 (April 8, 2013): 1097–108. http://dx.doi.org/10.1101/gr.151670.112.

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