Journal articles: 'Cancer cells metabolism'

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Pecqueur, Claire, Lisa Oliver, Kristell Oizel, Lisenn Lalier, and François M. Vallette. "Targeting Metabolism to Induce Cell Death in Cancer Cells and Cancer Stem Cells." International Journal of Cell Biology 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/805975.

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Abnormal metabolism and the evasion of apoptosis are considered hallmarks of cancers. Accumulating evidence shows that cancer stem cells are key drivers of tumor formation, progression, and recurrence. A successful therapy must therefore eliminate these cells known to be highly resistant to apoptosis. In this paper, we describe the metabolic changes as well as the mechanisms of resistance to apoptosis occurring in cancer cells and cancer stem cells, underlying the connection between these two processes.

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Annibaldi, Alessandro, and Christian Widmann. "Glucose metabolism in cancer cells." Current Opinion in Clinical Nutrition and Metabolic Care 13, no. 4 (July 2010): 466–70. http://dx.doi.org/10.1097/mco.0b013e32833a5577.

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Bekala, M. I. "ADAPTOR PROTEIN RUK/CIN85 IS INVOLVED IN THE GLUCOSE METABOLISM REPROGRAMMING IN BREAST CANCER CELLS." Biotechnologia Acta 15, no. 2 (April 2022): 47–48. http://dx.doi.org/10.15407/biotech15.02.047.

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Aim. This study aimed to investigate the changes in glucose metabolism in mouse 4T1 breast adenocarcinoma cells with different levels of Ruk/CIN85 expression. Methods. We used 4T1 cells with stable overexpression (subline RukUp) or knockdown (subline RukDown) of Ruk/CIN85, as well as corresponding vector control sublines Mock and Scr. Cells were cultured in the complete RPMI-1640 medium under standard conditions. mRNA expression levels were estimated by RT2-PCR, enzymes activities were measured by spectrophotometric and/or fluorometric assays. Results. Analysis of mRNA expression of glucose metabolism-related genes in RukUp and RukDown cells revealed that glycolysis genes are preferentially overexpressed in RukUp cells, and downregulated in RukDown cells. Thus, RukUp cells were characterized by significantly overexpressed Slc2a1, Gck, Aldoa, and Ldha, while in RukDown cells these genes were either down regulated or not changed. However, the expression of TCA (tricarboxylic acid) cycle enzyme Mdh2 increased dramatically (by 7,8 times) in RukDown cells. In detail, we observed statistically significant changes in the activity of all studied enzymes in RukUp cells (increase by 1,5-1,9 times for glycolysis enzymes and G6PD, and decrease by 1,33-1,69 times for TCA enzymes). However, in RukDown cells we did not find any significant changes in glycolysis enzymes activities, but activities of mitochondrial IDH3 and MDH2 were elevated by 1,65 and 1,59 times, respectively. Conclusions. The results obtained indicate that adaptor protein Ruk/CIN85 is involved in the metabolic reprogramming during breast cancer progression. High level of Ruk/CIN85 expression is associated with potentiation of the Warburg effect.

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Yan, Liang, Priyank Raj, Wantong Yao, and Haoqiang Ying. "Glucose Metabolism in Pancreatic Cancer." Cancers 11, no. 10 (September 29, 2019): 1460. http://dx.doi.org/10.3390/cancers11101460.

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Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and lethal cancers, with a five-year survival rate of around 5% to 8%. To date, very few available drugs have been successfully used to treat PDAC due to the poor understanding of the tumor-specific features. One of the hallmarks of pancreatic cancer cells is the deregulated cellular energetics characterized by the “Warburg effect”. It has been known for decades that cancer cells have a dramatically increased glycolytic flux even in the presence of oxygen and normal mitochondrial function. Glycolytic flux is the central carbon metabolism process in all cells, which not only produces adenosine triphosphate (ATP) but also provides biomass for anabolic processes that support cell proliferation. Expression levels of glucose transporters and rate-limiting enzymes regulate the rate of glycolytic flux. Intermediates that branch out from glycolysis are responsible for redox homeostasis, glycosylation, and biosynthesis. Beyond enhanced glycolytic flux, pancreatic cancer cells activate nutrient salvage pathways, which includes autophagy and micropinocytosis, from which the generated sugars, amino acids, and fatty acids are used to buffer the stresses induced by nutrient deprivation. Further, PDAC is characterized by extensive metabolic crosstalk between tumor cells and cells in the tumor microenvironment (TME). In this review, we will give an overview on recent progresses made in understanding glucose metabolism-related deregulations in PDAC.

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Saunders, F. R., and H. M. Wallace. "Polyamine metabolism and cancer prevention." Biochemical Society Transactions 35, no. 2 (March 20, 2007): 364–68. http://dx.doi.org/10.1042/bst0350364.

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Colorectal cancer is one of a number of cancers that may be amenable to prevention. The NSAIDs (non-steroidal anti-inflammatory drugs) have been shown to be effective chemopreventative agents in humans, but their mechanism of action is not clear. The polyamines are cellular polycations that are essential for cell growth and are overproduced in cancer cells. It is our hypothesis that inhibition of polyamine metabolism is an integral part of the mechanism of cancer prevention mediated by NSAIDs.

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Dutta, Anika, and Neelam Sharma-Walia. "Curbing Lipids: Impacts ON Cancer and Viral Infection." International Journal of Molecular Sciences 20, no. 3 (February 2, 2019): 644. http://dx.doi.org/10.3390/ijms20030644.

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Lipids play a fundamental role in maintaining normal function in healthy cells. Their functions include signaling, storing energy, and acting as the central structural component of cell membranes. Alteration of lipid metabolism is a prominent feature of cancer, as cancer cells must modify their metabolism to fulfill the demands of their accelerated proliferation rate. This aberrant lipid metabolism can affect cellular processes such as cell growth, survival, and migration. Besides the gene mutations, environmental factors, and inheritance, several infectious pathogens are also linked with human cancers worldwide. Tumor viruses are top on the list of infectious pathogens to cause human cancers. These viruses insert their own DNA (or RNA) into that of the host cell and affect host cellular processes such as cell growth, survival, and migration. Several of these cancer-causing viruses are reported to be reprogramming host cell lipid metabolism. The reliance of cancer cells and viruses on lipid metabolism suggests enzymes that can be used as therapeutic targets to exploit the addiction of infected diseased cells on lipids and abrogate tumor growth. This review focuses on normal lipid metabolism, lipid metabolic pathways and their reprogramming in human cancers and viral infection linked cancers and the potential anticancer drugs that target specific lipid metabolic enzymes. Here, we discuss statins and fibrates as drugs to intervene in disordered lipid pathways in cancer cells. Further insight into the dysregulated pathways in lipid metabolism can help create more effective anticancer therapies.

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Zhu, Xuan, Hui-Hui Chen, Chen-Yi Gao, Xin-Xin Zhang, Jing-Xin Jiang, Yi Zhang, Jun Fang, Feng Zhao, and Zhi-Gang Chen. "Energy metabolism in cancer stem cells." World Journal of Stem Cells 12, no. 6 (June 26, 2020): 448–61. http://dx.doi.org/10.4252/wjsc.v12.i6.448.

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Leone, Robert D., and Jonathan D. Powell. "Metabolism of immune cells in cancer." Nature Reviews Cancer 20, no. 9 (July 6, 2020): 516–31. http://dx.doi.org/10.1038/s41568-020-0273-y.

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Gough, N. R. "Rewiring the Metabolism of Cancer Cells." Science Signaling 7, no. 347 (October 14, 2014): ec282-ec282. http://dx.doi.org/10.1126/scisignal.aaa0412.

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Cao, Hui, and Jianbo Xiao. "Metabolism of stilbenoids in cancer cells." Free Radical Biology and Medicine 128 (November 2018): S81. http://dx.doi.org/10.1016/j.freeradbiomed.2018.10.181.

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DeBerardinis, Ralph J., and Navdeep S. Chandel. "Fundamentals of cancer metabolism." Science Advances 2, no. 5 (May 2016): e1600200. http://dx.doi.org/10.1126/sciadv.1600200.

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Tumors reprogram pathways of nutrient acquisition and metabolism to meet the bioenergetic, biosynthetic, and redox demands of malignant cells. These reprogrammed activities are now recognized as hallmarks of cancer, and recent work has uncovered remarkable flexibility in the specific pathways activated by tumor cells to support these key functions. In this perspective, we provide a conceptual framework to understand how and why metabolic reprogramming occurs in tumor cells, and the mechanisms linking altered metabolism to tumorigenesis and metastasis. Understanding these concepts will progressively support the development of new strategies to treat human cancer.

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Caneba, Christine A., Nadège Bellance, Lifeng Yang, Lisa Pabst, and Deepak Nagrath. "Pyruvate uptake is increased in highly invasive ovarian cancer cells under anoikis conditions for anaplerosis, mitochondrial function, and migration." American Journal of Physiology-Endocrinology and Metabolism 303, no. 8 (October 15, 2012): E1036—E1052. http://dx.doi.org/10.1152/ajpendo.00151.2012.

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Anoikis resistance, or the ability for cells to live detached from the extracellular matrix, is a property of epithelial cancers. The “Warburg effect,” or the preference of cancer cells for glycolysis for their energy production even in the presence of oxygen, has been shown to be evident in various tumors. Since a cancer cell's metastatic ability depends on microenvironmental conditions (nutrients, stromal cells, and vascularization) and is highly variable for different organs, their cellular metabolic fluxes and nutrient demand may show considerable differences. Moreover, a cancer cell's metastatic ability, which is dependent on the stage of cancer, may further create metabolic alterations depending on its microenvironment. Although recent studies have aimed to elucidate cancer cell metabolism under detached conditions, the nutrient demand and metabolic activity of cancer cells under nonadherent conditions remain poorly understood. Additionally, less is known about metabolic alterations in ovarian cancer cells with varying invasive capability under anoikis conditions. We hypothesized that the metabolism of highly invasive ovarian cancer cells in detachment would differ from less invasive ovarian cancer cells and that ovarian cancer cells will have altered metabolism in detached vs. attached conditions. To assess these metabolic differences, we integrated a secretomics-based metabolic footprinting (MFP) approach with mitochondrial bioenergetics. Interestingly, MFP revealed higher pyruvate uptake and oxygen consumption in more invasive ovarian cancer cells than their less invasive counterparts. Furthermore, ATP production was higher in more invasive vs. less invasive ovarian cancer cells in detachment. We found that pyruvate has an effect on highly invasive ovarian cancer cells' migration ability. Our results are the first to demonstrate that higher mitochondrial activity is related to higher ovarian cancer invasiveness under detached conditions. Importantly, our results bring insights regarding the metabolism of cancer cells under nonadherent conditions and could lead to the development of therapies for modulating cancer cell invasiveness.

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Ding, Shijie, Chunbao Li, Ninghui Cheng, Xiaojiang Cui, Xinglian Xu, and Guanghong Zhou. "Redox Regulation in Cancer Stem Cells." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/750798.

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Reactive oxygen species (ROS) and ROS-dependent (redox regulation) signaling pathways and transcriptional activities are thought to be critical in stem cell self-renewal and differentiation during growth and organogenesis. Aberrant ROS burst and dysregulation of those ROS-dependent cellular processes are strongly associated with human diseases including many cancers. ROS levels are elevated in cancer cells partially due to their higher metabolism rate. In the past 15 years, the concept of cancer stem cells (CSCs) has been gaining ground as the subpopulation of cancer cells with stem cell-like properties and characteristics have been identified in various cancers. CSCs possess low levels of ROS and are responsible for cancer recurrence after chemotherapy or radiotherapy. Unfortunately, how CSCs control ROS production and scavenging and how ROS-dependent signaling pathways contribute to CSCs function remain poorly understood. This review focuses on the role of redox balance, especially in ROS-dependent cellular processes in cancer stem cells (CSCs). We updated recent advances in our understanding of ROS generation and elimination in CSCs and their effects on CSC self-renewal and differentiation through modulating signaling pathways and transcriptional activities. The review concludes that targeting CSCs by manipulating ROS metabolism/dependent pathways may be an effective approach for improving cancer treatment.

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Reiter, Russel J. "Melatonin Reprograms Glucose Metabolism in Cancer Cell Mitochondria." Series of Endocrinology, Diabetes and Metabolism 1, no. 3 (October 9, 2019): 52–61. http://dx.doi.org/10.54178/jsedmv1i3001.

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Melatonin has a long history of studies which confirm its ability to inhibit cancer growth. Melatonin is present in high concentrations in the mitochondria of normal cells but is likely absent from the mitochondria of cancer cells, at least when isolated from tumors harvested during the day. Herein, we hypothesize that melatonin’s absence from cancer cell mitochondria prevents these organelles from metabolizing pyruvate to acetyl coenzyme A (acetyl-CoA) due to suppression of the activity of the enzyme pyruvate dehydrogenase complex (PDC), the enzyme that catalyzes the conversion of pyruvate to acetyl-CoA. This causes cancer cells to metabolize glucose to lactate in the cytosol (the Warburg effect). Since cancer cell mitochondria can take up nighttime pineal-derived melatonin from the blood, the indoleamine predictably promotes the conversion of pyruvate to acetyl-CoA in the mitochondria during the night. Thus, while cancer cells exhibit a typical cancer phenotype during the day, at night cancer cells have a more normal cell phenotype. Via similar actions, melatonin probably overcomes the insensitivity of cancers to chemotherapies. Hopefully, the hypothetical processes proposed herein will soon be experimentally tested.

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Shen, Yao-An, Chang-Cyuan Chen, Bo-Jung Chen, Yu-Ting Wu, Jiun-Ru Juan, Liang-Yun Chen, Yueh-Chun Teng, and Yau-Huei Wei. "Potential Therapies Targeting Metabolic Pathways in Cancer Stem Cells." Cells 10, no. 7 (July 13, 2021): 1772. http://dx.doi.org/10.3390/cells10071772.

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Cancer stem cells (CSCs) are heterogeneous cells with stem cell-like properties that are responsible for therapeutic resistance, recurrence, and metastasis, and are the major cause for cancer treatment failure. Since CSCs have distinct metabolic characteristics that plays an important role in cancer development and progression, targeting metabolic pathways of CSCs appears to be a promising therapeutic approach for cancer treatment. Here we classify and discuss the unique metabolisms that CSCs rely on for energy production and survival, including mitochondrial respiration, glycolysis, glutaminolysis, and fatty acid metabolism. Because of metabolic plasticity, CSCs can switch between these metabolisms to acquire energy for tumor progression in different microenvironments compare to the rest of tumor bulk. Thus, we highlight the specific conditions and factors that promote or suppress CSCs properties to portray distinct metabolic phenotypes that attribute to CSCs in common cancers. Identification and characterization of the features in these metabolisms can offer new anticancer opportunities and improve the prognosis of cancer. However, the therapeutic window of metabolic inhibitors used alone or in combination may be rather narrow due to cytotoxicity to normal cells. In this review, we present current findings of potential targets in these four metabolic pathways for the development of more effective and alternative strategies to eradicate CSCs and treat cancer more effectively in the future.

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Reyes-Castellanos, Gabriela, Rawand Masoud, and Alice Carrier. "Mitochondrial Metabolism in PDAC: From Better Knowledge to New Targeting Strategies." Biomedicines 8, no. 8 (August 3, 2020): 270. http://dx.doi.org/10.3390/biomedicines8080270.

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Cancer cells reprogram their metabolism to meet bioenergetics and biosynthetic demands. The first observation of metabolic reprogramming in cancer cells was made a century ago (“Warburg effect” or aerobic glycolysis), leading to the classical view that cancer metabolism relies on a glycolytic phenotype. There is now accumulating evidence that most cancers also rely on mitochondria to satisfy their metabolic needs. Indeed, the current view of cancer metabolism places mitochondria as key actors in all facets of cancer progression. Importantly, mitochondrial metabolism has become a very promising target in cancer therapy, including for refractory cancers such as Pancreatic Ductal AdenoCarcinoma (PDAC). In particular, mitochondrial oxidative phosphorylation (OXPHOS) is an important target in cancer therapy. Other therapeutic strategies include the targeting of glutamine and fatty acids metabolism, as well as the inhibition of the TriCarboxylic Acid (TCA) cycle intermediates. A better knowledge of how pancreatic cancer cells regulate mitochondrial metabolism will allow the identification of metabolic vulnerabilities and thus novel and more efficient therapeutic options for the benefit of each patient.

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Arfin, Saniya, Niraj Kumar Jha, Saurabh Kumar Jha, Kavindra Kumar Kesari, Janne Ruokolainen, Shubhadeep Roychoudhury, Brijesh Rathi, and Dhruv Kumar. "Oxidative Stress in Cancer Cell Metabolism." Antioxidants 10, no. 5 (April 22, 2021): 642. http://dx.doi.org/10.3390/antiox10050642.

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Reactive oxygen species (ROS) are important in regulating normal cellular processes whereas deregulated ROS leads to the development of a diseased state in humans including cancers. Several studies have been found to be marked with increased ROS production which activates pro-tumorigenic signaling, enhances cell survival and proliferation and drives DNA damage and genetic instability. However, higher ROS levels have been found to promote anti-tumorigenic signaling by initiating oxidative stress-induced tumor cell death. Tumor cells develop a mechanism where they adjust to the high ROS by expressing elevated levels of antioxidant proteins to detoxify them while maintaining pro-tumorigenic signaling and resistance to apoptosis. Therefore, ROS manipulation can be a potential target for cancer therapies as cancer cells present an altered redox balance in comparison to their normal counterparts. In this review, we aim to provide an overview of the generation and sources of ROS within tumor cells, ROS-associated signaling pathways, their regulation by antioxidant defense systems, as well as the effect of elevated ROS production in tumor progression. It will provide an insight into how pro- and anti-tumorigenic ROS signaling pathways could be manipulated during the treatment of cancer.

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Fasoulakis, Zacharias, Antonios Koutras, Thomas Ntounis, Ioannis Prokopakis, Paraskevas Perros, Athanasios Chionis, Ioakeim Sapantzoglou, et al. "Ovarian Cancer and Glutamine Metabolism." International Journal of Molecular Sciences 24, no. 5 (March 6, 2023): 5041. http://dx.doi.org/10.3390/ijms24055041.

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Cancer cells are known to have a distinct metabolic profile and to exhibit significant changes in a variety of metabolic mechanisms compared to normal cells, particularly glycolysis and glutaminolysis, in order to cover their increased energy requirements. There is mounting evidence that there is a link between glutamine metabolism and the proliferation of cancer cells, demonstrating that glutamine metabolism is a vital mechanism for all cellular processes, including the development of cancer. Detailed knowledge regarding its degree of engagement in numerous biological processes across distinct cancer types is still lacking, despite the fact that such knowledge is necessary for comprehending the differentiating characteristics of many forms of cancer. This review aims to examine data on glutamine metabolism and ovarian cancer and identify possible therapeutic targets for ovarian cancer treatment.

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Balzanelli, Mario G., Pietro Distratis, Rita Lazzaro, Van Hung Pham, Raffaele Del Prete, Adriana Mosca, Francesco Inchingolo, et al. "From Pathogens to Cancer: Are Cancer Cells Evolved Mitochondrial Super Cells?" Diagnostics 13, no. 4 (February 20, 2023): 813. http://dx.doi.org/10.3390/diagnostics13040813.

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Life is based on a highly specific combination of atoms, metabolism, and genetics which eventually reflects the chemistry of the Universe which is composed of hydrogen, oxygen, nitrogen, sulfur, phosphorus, and carbon. The interaction of atomic, metabolic, and genetic cycles results in the organization and de-organization of chemical information of that which we consider as living entities, including cancer cells. In order to approach the problem of the origin of cancer it is therefore reasonable to start from the assumption that the sub-molecular level, the atomic structure, should be the considered starting point on which metabolism, genetics, and external insults eventually emanate. Second, it is crucial to characterize which of the entities and parts composing human cells may live a separate life; certainly, this theoretical standpoint would consider mitochondria, an organelle of “bacteria” origin embedded in conditions favorable for the onset of both. This organelle has not only been tolerated by immunity but has also been placed as a central regulator of cell defense. Virus, bacteria, and mitochondria are also similar in the light of genetic and metabolic elements; they share not only equivalent DNA and RNA features but also many basic biological activities. Thus, it is important to finalize that once the cellular integrity has been constantly broken down, the mitochondria like any other virus or bacteria return to their original autonomy to simply survive. The Warburg’s law that states the ability of cancers to ferment glucose in the presence of oxygen, indicates mitochondria respiration abnormalities may be the underlying cause of this transformation towards super cancer cells. Though genetic events play a key part in altering biochemical metabolism, inducing aerobic glycolysis, this is not enough to impair mitochondrial function since mitochondrial biogenesis and quality control are constantly upregulated in cancers. While some cancers have mutations in the nuclear-encoded mitochondrial tricarboxylic acid (TCA) cycle, enzymes that produce oncogenic metabolites, there is also a bio-physic pathway for pathogenic mitochondrial genome mutations. The atomic level of all biological activities can be considered the very beginning, marked by the electron abnormal behavior that consequently affects DNA of both cells and mitochondria. Whilst the cell’s nucleus DNA after a certain number of errors and defection tends to gradually switch off, the mitochondria DNA starts adopting several escape strategies, switching-on a few important genes that belong back at their original roots as independent beings. The ability to adopt this survival trick, by becoming completely immune to current life-threatening events, is probably the beginning of a differentiation process towards a “super-power cell”, the cancer cells that remind many pathogens, including virus, bacteria, and fungi. Thus, here, we present a hypothesis regarding those changes that first begin at the mitochondria atomic level to steadily involve molecular, tissue and organ levels in response to the virus or bacteria constant insults that drive a mitochondria itself to become an “immortal cancer cell”. Improved insights into this interplay between these pathogens and mitochondria progression may disclose newly epistemological paradigms as well as innovative procedures in targeting cancer cell progressive invasion.

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Talty, Ronan, and Kelly Olino. "Metabolism of Innate Immune Cells in Cancer." Cancers 13, no. 4 (February 21, 2021): 904. http://dx.doi.org/10.3390/cancers13040904.

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Cancer cells possess specific metabolic requirements for their survival, proliferation, and progression. Within a shared microenvironment, immune cells depend on competing metabolic pathways for their development and effector function. As a result, local acidification, hypoxia, and nutrient depletion in the tumor microenvironment can alter the antitumor immune response and even promote resistance to immunotherapies such as immune checkpoint blockade and adoptive cell transfer. Although T cells are the primary effectors of the antitumor response, growing evidence demonstrates that innate immune cells are critical to successful tumor clearance. This review aims to summarize current research related to the innate immune system, metabolism, and cancer. We first discuss the specific metabolic requirements of innate immune cells for immune activation and suppression and conclude by highlighting ongoing clinical applications of these findings.

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Bergers, Gabriele, and Sarah-Maria Fendt. "The metabolism of cancer cells during metastasis." Nature Reviews Cancer 21, no. 3 (January 18, 2021): 162–80. http://dx.doi.org/10.1038/s41568-020-00320-2.

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Shahruzaman, Shazwin Hani, Sharida Fakurazi, and Sandra Maniam. "Targeting energy metabolism to eliminate cancer cells." Cancer Management and Research Volume 10 (July 2018): 2325–35. http://dx.doi.org/10.2147/cmar.s167424.

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Fiorelli, G., L. Picariello, V. Martineti, I. Tognarini, F. Tonelli, and M. L. Brandi. "Estrogen metabolism in human colorectal cancer cells." Journal of Steroid Biochemistry and Molecular Biology 81, no. 3 (July 2002): 281–89. http://dx.doi.org/10.1016/s0960-0760(02)00075-4.

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BAGGETTO, L. "Deviant energetic metabolism of glycolytic cancer cells." Biochimie 74, no. 11 (November 1992): 959–74. http://dx.doi.org/10.1016/0300-9084(92)90016-8.

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Yang, Mengqi, Panpan Liu, and Peng Huang. "Cancer stem cells, metabolism, and therapeutic significance." Tumor Biology 37, no. 5 (February 10, 2016): 5735–42. http://dx.doi.org/10.1007/s13277-016-4945-x.

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Hata, H., C. F. Holinka, S. L. Pahuja, R. B. Hochberg, H. Kuramoto, and E. Gurpide. "Estradiol metabolism in ishikawa endometrial cancer cells." Journal of Steroid Biochemistry 26, no. 6 (June 1987): 699–704. http://dx.doi.org/10.1016/0022-4731(87)91042-9.

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Mattaini, Katherine R., Mark R. Sullivan, and Matthew G. Vander Heiden. "The importance of serine metabolism in cancer." Journal of Cell Biology 214, no. 3 (July 25, 2016): 249–57. http://dx.doi.org/10.1083/jcb.201604085.

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Serine metabolism is frequently dysregulated in cancers; however, the benefit that this confers to tumors remains controversial. In many cases, extracellular serine alone is sufficient to support cancer cell proliferation, whereas some cancer cells increase serine synthesis from glucose and require de novo serine synthesis even in the presence of abundant extracellular serine. Recent studies cast new light on the role of serine metabolism in cancer, suggesting that active serine synthesis might be required to facilitate amino acid transport, nucleotide synthesis, folate metabolism, and redox homeostasis in a manner that impacts cancer.

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Anastasiou, Dimitrios. "Metabolic reprogramming in cancer cells." Biochemist 37, no. 1 (February 1, 2015): 24–28. http://dx.doi.org/10.1042/bio03701024.

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Metabolism is fundamental for life as it provides organisms with a means to utilize nutrients from their environment for production of energy and biosynthetic precursors to support cellular functions. Despite a large body of knowledge that describes how different metabolites interconvert through a labyrinth of chemical reactions, how metabolic changes contribute to disease is not sufficiently well understood. Growing evidence suggests that metabolic alterations have important roles in tumorigenesis. Therefore elucidating the roles of metabolism in cancer holds significant promise for the development of new therapeutic avenues.

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Vettore, Lisa, Rebecca L. Westbrook, and Daniel A. Tennant. "New aspects of amino acid metabolism in cancer." British Journal of Cancer 122, no. 2 (December 10, 2019): 150–56. http://dx.doi.org/10.1038/s41416-019-0620-5.

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AbstractAn abundant supply of amino acids is important for cancers to sustain their proliferative drive. Alongside their direct role as substrates for protein synthesis, they can have roles in energy generation, driving the synthesis of nucleosides and maintenance of cellular redox homoeostasis. As cancer cells exist within a complex and often nutrient-poor microenvironment, they sometimes exist as part of a metabolic community, forming relationships that can be both symbiotic and parasitic. Indeed, this is particularly evident in cancers that are auxotrophic for particular amino acids. This review discusses the stromal/cancer cell relationship, by using examples to illustrate a number of different ways in which cancer cells can rely on and contribute to their microenvironment – both as a stable network and in response to therapy. In addition, it examines situations when amino acid synthesis is driven through metabolic coupling to other reactions, and synthesis is in excess of the cancer cell’s proliferative demand. Finally, it highlights the understudied area of non-proteinogenic amino acids in cancer metabolism and their potential role.

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Mushtaq, Muhammad, Suhas Darekar, and Elena Kashuba. "DNA Tumor Viruses and Cell Metabolism." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/6468342.

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Viruses play an important role in cancerogenesis. It is estimated that approximately 20% of all cancers are linked to infectious agents. The viral genes modulate the physiological machinery of infected cells that lead to cell transformation and development of cancer. One of the important adoptive responses by the cancer cells is their metabolic change to cope up with continuous requirement of cell survival and proliferation. In this review we will focus on how DNA viruses alter the glucose metabolism of transformed cells. Tumor DNA viruses enhance “aerobic” glycolysis upon virus-induced cell transformation, supporting rapid cell proliferation and showing the Warburg effect. Moreover, viral proteins enhance glucose uptake and controls tumor microenvironment, promoting metastasizing of the tumor cells.

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Kubik, Joanna, Ewelina Humeniuk, Grzegorz Adamczuk, Barbara Madej-Czerwonka, and Agnieszka Korga-Plewko. "Targeting Energy Metabolism in Cancer Treatment." International Journal of Molecular Sciences 23, no. 10 (May 16, 2022): 5572. http://dx.doi.org/10.3390/ijms23105572.

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Cancer is the second most common cause of death worldwide after cardiovascular diseases. The development of molecular and biochemical techniques has expanded the knowledge of changes occurring in specific metabolic pathways of cancer cells. Increased aerobic glycolysis, the promotion of anaplerotic responses, and especially the dependence of cells on glutamine and fatty acid metabolism have become subjects of study. Despite many cancer treatment strategies, many patients with neoplastic diseases cannot be completely cured due to the development of resistance in cancer cells to currently used therapeutic approaches. It is now becoming a priority to develop new treatment strategies that are highly effective and have few side effects. In this review, we present the current knowledge of the enzymes involved in the different steps of glycolysis, the Krebs cycle, and the pentose phosphate pathway, and possible targeted therapies. The review also focuses on presenting the differences between cancer cells and normal cells in terms of metabolic phenotype. Knowledge of cancer cell metabolism is constantly evolving, and further research is needed to develop new strategies for anti-cancer therapies.

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Forciniti, Stefania, Luana Greco, Fabio Grizzi, Alberto Malesci, and Luigi Laghi. "Iron Metabolism in Cancer Progression." International Journal of Molecular Sciences 21, no. 6 (March 24, 2020): 2257. http://dx.doi.org/10.3390/ijms21062257.

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Iron is indispensable for cell metabolism of both normal and cancer cells. In the latter, several disruptions of its metabolism occur at the steps of tumor initiation, progression and metastasis. Noticeably, cancer cells require a large amount of iron, and exhibit a strong dependence on it for their proliferation. Numerous iron metabolism-related proteins and signaling pathways are altered by iron in malignancies, displaying the pivotal role of iron in cancer. Iron homeostasis is regulated at several levels, from absorption by enterocytes to recycling by macrophages and storage in hepatocytes. Mutations in HFE gene alter iron homeostasis leading to hereditary hemochromatosis and to an increased cancer risk because the accumulation of iron induces oxidative DNA damage and free radical activity. Additionally, the iron capability to modulate immune responses is pivotal in cancer progression. Macrophages show an iron release phenotype and potentially deliver iron to cancer cells, resulting in tumor promotion. Overall, alterations in iron metabolism are among the metabolic and immunological hallmarks of cancer, and further studies are required to dissect how perturbations of this element relate to tumor development and progression.

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Tanasova, Marina, Vagarshak V. Begoyan, and Lukasz J. Weselinski. "Targeting Sugar Uptake and Metabolism for Cancer Identification and Therapy: An Overview." Current Topics in Medicinal Chemistry 18, no. 6 (June 28, 2018): 467–83. http://dx.doi.org/10.2174/1568026618666180523110837.

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Metabolic deregulations have emerged as a cancer characteristic, opening a broad avenue for strategies and tools to target cancer through sugar uptake and metabolism. High expression levels of sugar transporters in cancer cells offered glycoconjugation as an approach to achieve enhanced cellular accumulation of drugs and imaging agents, with the sugar moiety anchoring the bioactive cargo to cancer cells. On the other hand, high demand for sugar nutrients in cancers provided a new avenue to target cancer cells with metabolic or sugar uptake inhibitors to induce cancer cells starvation or death. This overview summarizes recent advances in targeting cancer cells through sugar transport for cancer detection and therapy.

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Chatterjee, Payal, Mukesh Yadav, Namrata Chauhan, Ying Huang, and Yun Luo. "Cancer Cell Metabolism Featuring Nrf2." Current Drug Discovery Technologies 17, no. 3 (July 15, 2020): 263–71. http://dx.doi.org/10.2174/1570163815666180911092443.

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Although the major role of Nrf2 has long been established as a transcription factor for providing cellular protection against oxidative stress, multiple pieces of research and reviews now claim exactly the opposite. The dilemma - “to activate or inhibit” the protein requires an immediate answer, which evidently links cellular metabolism to the causes and purpose of cancer. Profusely growing cancerous cells have prolific energy requirements, which can only be fulfilled by modulating cellular metabolism. This review highlights the cause and effect of Nrf2 modulation in cancer that in turn channelize cellular metabolism, thereby fulfilling the energy requirements of cancer cells. The present work also highlights the purpose of genetic mutations in Nrf2, in relation to cellular metabolism in cancer cells, thus pointing out a newer approach where parallel mutations may be the key factor to decide whether to activate or inhibit Nrf2.

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Smith, Danielle G., and Roger G. Sturmey. "Parallels between embryo and cancer cell metabolism." Biochemical Society Transactions 41, no. 2 (March 21, 2013): 664–69. http://dx.doi.org/10.1042/bst20120352.

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A key characteristic of cancer cells is the ability to switch from a predominantly oxidative metabolism to glycolysis and the production of lactate even when oxygen is plentiful. This metabolic switch, known as the Warburg effect, was first described in the 1920s, and has fascinated and puzzled researchers ever since. However, a dramatic increase in glycolysis in the presence of oxygen is one of the hallmarks of the development of the early mammalian embryo; a metabolic switch with many parallels to the Warburg effect of cancers. The present review provides a brief overview of this and other similarities between the metabolism in tumours and early embryos and proposes whether knowledge of early embryo metabolism can help us to understand metabolic regulation in cancer cells.

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Farhadi, Pegah, Reza Yarani, Sadat Dokaneheifard, and Kamran Mansouri. "The emerging role of targeting cancer metabolism for cancer therapy." Tumor Biology 42, no. 10 (October 2020): 101042832096528. http://dx.doi.org/10.1177/1010428320965284.

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Glucose, as the main consuming nutrient of the body, faces different destinies in cancer cells. Glycolysis, oxidative phosphorylation, and pentose phosphate pathways produce different glucose-derived metabolites and thus affect cells’ bioenergetics differently. Tumor cells’ dependency to aerobic glycolysis and other cancer-specific metabolism changes are known as the cancer hallmarks, distinct cancer cells from normal cells. Therefore, these tumor-specific characteristics receive the limelight as targets for cancer therapy. Glutamine, serine, and fatty acid oxidation together with 5-lipoxygenase are main pathways that have attracted lots of attention for cancer therapy. In this review, we not only discuss different tumor metabolism aspects but also discuss the metabolism roles in the promotion of cancer cells at different stages and their difference with normal cells. Besides, we dissect the inhibitors potential in blocking the main metabolic pathways to introduce the effective and non-effective inhibitors in the field.

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Skuli, Sarah J., Safwan Alomari, Hallie Gaitsch, A’ishah Bakayoko, Nicolas Skuli, and Betty M. Tyler. "Metformin and Cancer, an Ambiguanidous Relationship." Pharmaceuticals 15, no. 5 (May 19, 2022): 626. http://dx.doi.org/10.3390/ph15050626.

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The deregulation of energetic and cellular metabolism is a signature of cancer cells. Thus, drugs targeting cancer cell metabolism may have promising therapeutic potential. Previous reports demonstrate that the widely used normoglycemic agent, metformin, can decrease the risk of cancer in type 2 diabetics and inhibit cell growth in various cancers, including pancreatic, colon, prostate, ovarian, and breast cancer. While metformin is a known adenosine monophosphate-activated protein kinase (AMPK) agonist and an inhibitor of the electron transport chain complex I, its mechanism of action in cancer cells as well as its effect on cancer metabolism is not clearly established. In this review, we will give an update on the role of metformin as an antitumoral agent and detail relevant evidence on the potential use and mechanisms of action of metformin in cancer. Analyzing antitumoral, signaling, and metabolic impacts of metformin on cancer cells may provide promising new therapeutic strategies in oncology.

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Lee, Eugene K., Karim Pirani, Jeffrey M. Holzbeierlein, Paige Martin, Parthasarathy Rangarajan, Jill Hamilton-Reeves, and Shrikant Anant. "Glucose metabolism and bladder cancer." Journal of Clinical Oncology 35, no. 6_suppl (February 20, 2017): 359. http://dx.doi.org/10.1200/jco.2017.35.6_suppl.359.

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359 Background: To understand and evaluate the role of glucose metabolism in bladder cancer growth, in the identification of disease, and development of potential treatment strategies. Methods: UMUC3, T24 and 253JBV cells were grown in varying glucose concentrations (25, 100 and 200mg/dl) and cell proliferation assay with Vi-Cell was performed. Next, we used Qiagen PCR array of glucose metabolic pathway of the UMUC3 cell line under different glucose concentrations. PKM2 is a driver of glycolysis and exists in an inactive dimer or active tetramer. Dimer PKM2 also known as Tumor M2-PK was measured in urine samples of bladder cancer patients using a commercially available ELISA kit (ScheBo Biotech AG). Lastly, Shikonin, a PKM2 inhibitor was evaluated as an inhibitor of bladder cancer cell proliferation using Vi-Cell. Results: Increased glucose concentration 200mg/dl leads to increased proliferation in bladder cancer cells while decreased concentration of glucose; 25mg/dl reduces proliferation compared to control (100). PCR array demonstrates genes in the glycolytic pathway genes are upregulated in cells that are grown in 200mg/dl glucose media and the TCA cycle genes are upregulated in cells that are subjected to the 25mg/dl glucose media when compared to control (100mg/dl). The enzyme pyruvate kinase M2 (PKM2) controls the transition from the glycolytic pathway to TCA cycle. We have found that 9/10 (90%) of bladder cancer urine samples show elevated levels of tumor M2-PK (>104) compared to urine from two normal subjects (~30 units ) using a commercially available ELISA kit. Conclusions: Increased glucose concentration 200mg/dl leads to increased proliferation in bladder cancer cells while decreased concentration of glucose; 25mg/dl reduces proliferation compared to control (100).

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Kumari, Sonam, Mohammed Sikander, Shabnam Malik, Manish K. Tripathi, Bilal B. Hafeez, Murali M. Yallapu, Subhash C. Chauhan, Sheema Khan, and Meena Jaggi. "Steviol Represses Glucose Metabolism and Translation Initiation in Pancreatic Cancer Cells." Biomedicines 9, no. 12 (December 2, 2021): 1814. http://dx.doi.org/10.3390/biomedicines9121814.

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Pancreatic cancer has the worst prognosis and lowest survival rate among all cancers. Pancreatic cancer cells are highly metabolically active and typically reprogrammed for aberrant glucose metabolism; thus they respond poorly to therapeutic modalities. It is highly imperative to understand mechanisms that are responsible for high glucose metabolism and identify natural/synthetic agents that can repress glucose metabolic machinery in pancreatic cancer cells, to improve the therapeutic outcomes/management of pancreatic cancer patients. We have identified a glycoside, steviol that effectively represses glucose consumption in pancreatic cancer cells via the inhibition of the translation initiation machinery of the molecular components. Herein, we report that steviol effectively inhibits the glucose uptake and lactate production in pancreatic cancer cells (AsPC1 and HPAF-II). The growth, colonization, and invasion characteristics of pancreatic cancer cells were also determined by in vitro functional assay. Steviol treatment also inhibited the tumorigenic and metastatic potential of human pancreatic cancer cells by inducing apoptosis and cell cycle arrest in the G1/M phase. The metabolic shift by steviol was mediated through the repression of the phosphorylation of mTOR and translation initiation proteins (4E-BP1, eIF4e, eIF4B, and eIF4G). Overall, the results of this study suggest that steviol can effectively suppress the glucose metabolism and translation initiation in pancreatic cancer cells to mitigate their aggressiveness. This study might help in the design of newer combination therapeutic strategies for pancreatic cancer treatment.

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Rodríguez-Enríquez, Sara, Álvaro Marín-Hernández, Juan Carlos Gallardo-Pérez, Silvia Cecilia Pacheco-Velázquez, Javier Alejandro Belmont-Díaz, Diana Xochiquetzal Robledo-Cadena, Jorge Luis Vargas-Navarro, Norma Angélica Corona de la Peña, Emma Saavedra, and Rafael Moreno-Sánchez. "Transcriptional Regulation of Energy Metabolism in Cancer Cells." Cells 8, no. 10 (October 9, 2019): 1225. http://dx.doi.org/10.3390/cells8101225.

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Cancer development, growth, and metastasis are highly regulated by several transcription regulators (TRs), namely transcription factors, oncogenes, tumor-suppressor genes, and protein kinases. Although TR roles in these events have been well characterized, their functions in regulating other important cancer cell processes, such as metabolism, have not been systematically examined. In this review, we describe, analyze, and strive to reconstruct the regulatory networks of several TRs acting in the energy metabolism pathways, glycolysis (and its main branching reactions), and oxidative phosphorylation of nonmetastatic and metastatic cancer cells. Moreover, we propose which possible gene targets might allow these TRs to facilitate the modulation of each energy metabolism pathway, depending on the tumor microenvironment.

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Karta, Jessica, Ysaline Bossicard, Konstantinos Kotzamanis, Helmut Dolznig, and Elisabeth Letellier. "Mapping the Metabolic Networks of Tumor Cells and Cancer-Associated Fibroblasts." Cells 10, no. 2 (February 2, 2021): 304. http://dx.doi.org/10.3390/cells10020304.

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Metabolism is considered to be the core of all cellular activity. Thus, extensive studies of metabolic processes are ongoing in various fields of biology, including cancer research. Cancer cells are known to adapt their metabolism to sustain high proliferation rates and survive in unfavorable environments with low oxygen and nutrient concentrations. Hence, targeting cancer cell metabolism is a promising therapeutic strategy in cancer research. However, cancers consist not only of genetically altered tumor cells but are interwoven with endothelial cells, immune cells and fibroblasts, which together with the extracellular matrix (ECM) constitute the tumor microenvironment (TME). Cancer-associated fibroblasts (CAFs), which are linked to poor prognosis in different cancer types, are one important component of the TME. CAFs play a significant role in reprogramming the metabolic landscape of tumor cells, but how, and in what manner, this interaction takes place remains rather unclear. This review aims to highlight the metabolic landscape of tumor cells and CAFs, including their recently identified subtypes, in different tumor types. In addition, we discuss various in vitro and in vivo metabolic techniques as well as different in silico computational tools that can be used to identify and characterize CAF–tumor cell interactions. Finally, we provide our view on how mapping the complex metabolic networks of stromal-tumor metabolism will help in finding novel metabolic targets for cancer treatment.

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Mamouni, Kenza, Georgios Kallifatidis, and Bal L. Lokeshwar. "Targeting Mitochondrial Metabolism in Prostate Cancer with Triterpenoids." International Journal of Molecular Sciences 22, no. 5 (February 28, 2021): 2466. http://dx.doi.org/10.3390/ijms22052466.

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Metabolic reprogramming is a hallmark of malignancy. It implements profound metabolic changes to sustain cancer cell survival and proliferation. Although the Warburg effect is a common feature of metabolic reprogramming, recent studies have revealed that tumor cells also depend on mitochondrial metabolism. Due to the essential role of mitochondria in metabolism and cell survival, targeting mitochondria in cancer cells is an attractive therapeutic strategy. However, the metabolic flexibility of cancer cells may enable the upregulation of compensatory pathways, such as glycolysis, to support cancer cell survival when mitochondrial metabolism is inhibited. Thus, compounds capable of targeting both mitochondrial metabolism and glycolysis may help overcome such resistance mechanisms. Normal prostate epithelial cells have a distinct metabolism as they use glucose to sustain physiological citrate secretion. During the transformation process, prostate cancer cells consume citrate to mainly power oxidative phosphorylation and fuel lipogenesis. A growing number of studies have assessed the impact of triterpenoids on prostate cancer metabolism, underlining their ability to hit different metabolic targets. In this review, we critically assess the metabolic transformations occurring in prostate cancer cells. We will then address the opportunities and challenges in using triterpenoids as modulators of prostate cancer cell metabolism.

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Choudhury, Feroza K. "Mitochondrial Redox Metabolism: The Epicenter of Metabolism during Cancer Progression." Antioxidants 10, no. 11 (November 19, 2021): 1838. http://dx.doi.org/10.3390/antiox10111838.

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Mitochondrial redox metabolism is the central component in the cellular metabolic landscape, where anabolic and catabolic pathways are reprogrammed to maintain optimum redox homeostasis. During different stages of cancer, the mitochondrial redox status plays an active role in navigating cancer cells’ progression and regulating metabolic adaptation according to the constraints of each stage. Mitochondrial reactive oxygen species (ROS) accumulation induces malignant transformation. Once vigorous cell proliferation renders the core of the solid tumor hypoxic, the mitochondrial electron transport chain mediates ROS signaling for bringing about cellular adaptation to hypoxia. Highly aggressive cells are selected in this process, which are capable of progressing through the enhanced oxidative stress encountered during different stages of metastasis for distant colonization. Mitochondrial oxidative metabolism is suppressed to lower ROS generation, and the overall cellular metabolism is reprogrammed to maintain the optimum NADPH level in the mitochondria required for redox homeostasis. After reaching the distant organ, the intrinsic metabolic limitations of that organ dictate the success of colonization and flexibility of the mitochondrial metabolism of cancer cells plays a pivotal role in their adaptation to the new environment.

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Hamanaka, Robert B., and Navdeep S. Chandel. "Targeting glucose metabolism for cancer therapy." Journal of Experimental Medicine 209, no. 2 (February 13, 2012): 211–15. http://dx.doi.org/10.1084/jem.20120162.

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Cellular transformation is associated with the reprogramming of cellular pathways that control proliferation, survival, and metabolism. Among the metabolic changes exhibited by tumor cells is an increase in glucose metabolism and glucose dependence. It has been hypothesized that targeting glucose metabolism may provide a selective mechanism by which to kill cancer cells. In this minireview, we discuss the benefits that high levels of glycolysis provide for tumor cells, as well as several key enzymes required by cancer cells to maintain this high level of glucose metabolism. It is anticipated that understanding which metabolic enzymes are particularly critical for tumor cell proliferation and survival will identify novel therapeutic targets.

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Chartoumpekis, Dionysios V., Nobunao Wakabayashi, and Thomas W. Kensler. "Keap1/Nrf2 pathway in the frontiers of cancer and non-cancer cell metabolism." Biochemical Society Transactions 43, no. 4 (August 1, 2015): 639–44. http://dx.doi.org/10.1042/bst20150049.

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Cancer cells adapt their metabolism to their increased needs for energy and substrates for protein, lipid and nucleic acid synthesis. Nuclear erythroid factor 2-like 2 (Nrf2) pathway is usually activated in cancers and has been suggested to promote cancer cell survival mainly by inducing a large battery of cytoprotective genes. This mini review focuses on metabolic pathways, beyond cytoprotection, which can be directly or indirectly regulated by Nrf2 in cancer cells to affect their survival. The pentose phosphate pathway (PPP) is enhanced by Nrf2 in cancers and aids their growth. PPP has also been found to be up-regulated in non-cancer tissues and other pathways, such as de novo lipogenesis, have been found to be repressed after activation of the Nrf2 pathway. The importance of these Nrf2-regulated metabolic pathways in cancer compared with non-cancer state remains to be determined. Last but not least, the importance of context about Nrf2 and cancer is highlighted as the Nrf2 pathway may be activated in cancers but its pharmacological activators are useful in chemoprevention.

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Kim, Go Woon, Dong Hoon Lee, Yu Hyun Jeon, Jung Yoo, So Yeon Kim, Sang Wu Lee, Ha Young Cho, and So Hee Kwon. "Glutamine Synthetase as a Therapeutic Target for Cancer Treatment." International Journal of Molecular Sciences 22, no. 4 (February 8, 2021): 1701. http://dx.doi.org/10.3390/ijms22041701.

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The significance of glutamine in cancer metabolism has been extensively studied. Cancer cells consume an excessive amount of glutamine to facilitate rapid proliferation. Thus, glutamine depletion occurs in various cancer types, especially in poorly vascularized cancers. This makes glutamine synthetase (GS), the only enzyme responsible for de novo synthesizing glutamine, essential in cancer metabolism. In cancer, GS exhibits pro-tumoral features by synthesizing glutamine, supporting nucleotide synthesis. Furthermore, GS is highly expressed in the tumor microenvironment (TME) and provides glutamine to cancer cells, allowing cancer cells to maintain sufficient glutamine level for glutamine catabolism. Glutamine catabolism, the opposite reaction of glutamine synthesis by GS, is well known for supporting cancer cell proliferation via contributing biosynthesis of various essential molecules and energy production. Either glutamine anabolism or catabolism has a critical function in cancer metabolism depending on the complex nature and microenvironment of cancers. In this review, we focus on the role of GS in a variety of cancer types and microenvironments and highlight the mechanism of GS at the transcriptional and post-translational levels. Lastly, we discuss the therapeutic implications of targeting GS in cancer.

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Li, Jiaqi, Jie Qing Eu, Li Ren Kong, Lingzhi Wang, Yaw Chyn Lim, Boon Cher Goh, and Andrea L. A. Wong. "Targeting Metabolism in Cancer Cells and the Tumour Microenvironment for Cancer Therapy." Molecules 25, no. 20 (October 20, 2020): 4831. http://dx.doi.org/10.3390/molecules25204831.

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Targeting altered tumour metabolism is an emerging therapeutic strategy for cancer treatment. The metabolic reprogramming that accompanies the development of malignancy creates targetable differences between cancer cells and normal cells, which may be exploited for therapy. There is also emerging evidence regarding the role of stromal components, creating an intricate metabolic network consisting of cancer cells, cancer-associated fibroblasts, endothelial cells, immune cells, and cancer stem cells. This metabolic rewiring and crosstalk with the tumour microenvironment play a key role in cell proliferation, metastasis, and the development of treatment resistance. In this review, we will discuss therapeutic opportunities, which arise from dysregulated metabolism and metabolic crosstalk, highlighting strategies that may aid in the precision targeting of altered tumour metabolism with a focus on combinatorial therapeutic strategies.

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Wen, Gui-Min, Xiao-Yan Xu, and Pu Xia. "Metabolism in Cancer Stem Cells: Targets for Clinical Treatment." Cells 11, no. 23 (November 26, 2022): 3790. http://dx.doi.org/10.3390/cells11233790.

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Cancer stem cells (CSCs) have high tumorigenicity, high metastasis and high resistance to treatment. They are the key factors for the growth, metastasis and drug resistance of malignant tumors, and are also the important reason for the occurrence and recurrence of tumors. Metabolic reprogramming refers to the metabolic changes that occur when tumor cells provide sufficient energy and nutrients for themselves. Metabolic reprogramming plays an important role in regulating the growth and activity of cancer cells and cancer stem cells. In addition, the immune cells or stromal cells in the tumor microenvironment (TME) will change due to the metabolic reprogramming of cancer cells. Summarizing the characteristics and molecular mechanisms of metabolic reprogramming of cancer stem cells will provide new ideas for the comprehensive treatment of malignant tumors. In this review, we summarized the changes of the main metabolic pathways in cancer cells and cancer stem cells.

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El-Sahli, Sara, Ying Xie, Lisheng Wang, and Sheng Liu. "Wnt Signaling in Cancer Metabolism and Immunity." Cancers 11, no. 7 (June 28, 2019): 904. http://dx.doi.org/10.3390/cancers11070904.

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The Wingless (Wnt)/β-catenin pathway has long been associated with tumorigenesis, tumor plasticity, and tumor-initiating cells called cancer stem cells (CSCs). Wnt signaling has recently been implicated in the metabolic reprogramming of cancer cells. Aberrant Wnt signaling is considered to be a driver of metabolic alterations of glycolysis, glutaminolysis, and lipogenesis, processes essential to the survival of bulk and CSC populations. Over the past decade, the Wnt pathway has also been shown to regulate the tumor microenvironment (TME) and anti-cancer immunity. Wnt ligands released by tumor cells in the TME facilitate the immune evasion of cancer cells and hamper immunotherapy. In this review, we illustrate the role of the canonical Wnt/β-catenin pathway in cancer metabolism and immunity to explore the potential therapeutic approach of targeting Wnt signaling from a metabolic and immunological perspective.

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Smetana, Karel, and Michal Masařík. "Advances in Cancer Metabolism and Tumour Microenvironment." International Journal of Molecular Sciences 23, no. 8 (April 7, 2022): 4071. http://dx.doi.org/10.3390/ijms23084071.

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Cancer represents an extremely complicated ecosystem where cancer cells communicate with non-cancer cells present in the tumour niche through intercellular contacts, paracrine production of bioactive factors and extracellular vesicles, such as exosomes [...]

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Journal articles on the topic 'Cancer cells metabolism'

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