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The Control of the Metabolic Switch in Cancers by Oncogenes and Tumor
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TLDR
Cells from some tumors use an altered metabolic pattern compared with that of normal differentiated adult cells in the body, which provides substrates for cell growth and division and free energy (ATP) from enhanced glucose use.Abstract:
Cells from some tumors use an altered metabolic pattern compared with that of normal differentiated adult cells in the body. Tumor cells take up much more glucose and mainly process it through aerobic glycolysis, producing large quantities of secreted lactate with a lower use of oxidative phosphorylation that would generate more adenosine triphosphate (ATP), water, and carbon dioxide. This is the Warburg effect, which provides substrates for cell growth and division and free energy (ATP) from enhanced glucose use. This metabolic switch places the emphasis on producing intermediates for cell growth and division, and it is regulated by both oncogenes and tumor suppressor genes in a number of key cancer-producing pathways. Blocking these metabolic pathways or restoring these altered pathways could lead to a new approach in cancer treatments.read more
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Roles of autophagy and metabolism in pancreatic cancer cell adaptation to environmental challenges
Sandrina Maertin,Jason M. Elperin,Jason M. Elperin,Ethan Lotshaw,Ethan Lotshaw,Matthias Sendler,Steven Speakman,Steven Speakman,Kazuki Takakura,Kazuki Takakura,Benjamin Reicher,Benjamin Reicher,Olga A. Mareninova,Olga A. Mareninova,Paul J. Grippo,Julia Mayerle,Markus M. Lerch,Anna S. Gukovskaya +17 more
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p53/BNIP3-dependent mitophagy limits glycolytic shift in radioresistant cancer.
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TL;DR: A previously unappreciated link between p53 and mitophagy was identified, which limited the glycolytic shift through the BNIP3-dependent clearance of abnormal mitochondria, which means drugs targeting glyCOlysis could be used as an alternative strategy for overcoming radioresistant cancers.
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Aldolase B suppresses hepatocellular carcinogenesis by inhibiting G6PD and pentose phosphate pathways
Min Li,Xuxiao He,Wei-Xing Guo,Hongming Yu,Shicheng Zhang,Shicheng Zhang,Ningning Wang,Guijun Liu,Rina Sa,Xia Shen,Xia Shen,Ya-Bo Jiang,Yufu Tang,Yujuan Zhuo,Yujuan Zhuo,Chunzhao Yin,Chunzhao Yin,Qiaochu Tu,Qiaochu Tu,Nan Li,Xiaoqun Nie,Yu Li,Zhimin Hu,Hanwen Zhu,Hanwen Zhu,Jianping Ding,Zi Li,Te Liu,Fan Zhang,He Zhou,Shengxian Li,Jiang Yue,Zheng Yan,Shu-Qun Cheng,Yongzhen Tao,Huiyong Yin +35 more
TL;DR: It is shown that hepatic aldolase B (Aldob) suppresses HCC by directly binding and inhibiting the rate-limiting enzyme in the pentose phosphate pathway, glucose-6-phosphate dehydrogenase (G6PD).
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Mitochondria and familial predisposition to breast cancer.
TL;DR: Since mitochondrial DNA is maternally inherited, hereditary breast cancer has been focused on and the involvement of mitochondrial DNA in cancer and in particular in breast cancer is examined.
References
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