'Warburg effect' controls tumor growth, bacterial, viral infections and immunity - Genetic deconstruction and therapeutic perspectives.
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In this paper , the Warburg effect via CRISPR-Cas9 disruption of glucose-6-phosphate isomerase (GPI-KO) or lactate dehydrogenases (LDHA/B-DKO) is revisited.About:
This article is published in Seminars in Cancer Biology.The article was published on 2022-07-01 and is currently open access. It has received 28 citations till now. The article focuses on the topics: Medicine & Warburg effect.read more
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Glycolysis in tumor microenvironment as a target to improve cancer immunotherapy
Chunyi Xiao,He Tian,Yujia Zheng,Zhenlin Wang,Shuofeng Li,Tao Fan,Jiachen Xu,Guangyu Bai,Jingjing Liu,Ziqin Deng,Chunxiang Li,Jie He +11 more
TL;DR: The glycolytic remodeling of various immune cells within the tumor microenvironment (TME) and the deleterious effects of limited nutrients and acidification derived from enhanced tumor glyCOlysis on immunological anti-tumor capacity are described.
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Hypoxic microenvironment in cancer: molecular mechanisms and therapeutic interventions
TL;DR: In this paper , the authors investigated the potential factors in the development of hypoxia in cancer, changes in signaling pathways that occur in cancer cells to adapt to hypoxic environments, the mechanisms of hypoxide-induced cancer immune tolerance, chemotherapeutic tolerance, and enhanced radiation tolerance, as well as the insights and applications of hypoxygenation in cancer therapy.
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Modulating Glycolysis to Improve Cancer Therapy
TL;DR: In this paper , the authors reviewed the role of metabolic reprogramming in cancer cells and how targeting this phenomenon could be a potential strategy to improve the efficacy of conventional cancer therapy.
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Beyond basic research: the contribution of cathepsin B to cancer development, diagnosis and therapy
TL;DR: A review of the literature that has justified or shaped the importance of CtsB expression in cancer progression, from the perspective of highlighting a paradigm that is rapidly changing from basic research toward a broader clinical and translational context is presented in this paper .
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Hyperforin Elicits Cytostatic/Cytotoxic Activity in Human Melanoma Cell Lines, Inhibiting Pro-Survival NF-κB, STAT3, AP1 Transcription Factors and the Expression of Functional Proteins Involved in Mitochondrial and Cytosolic Metabolism
Alessia Cardile,Valentina Zanrè,Rachele Campagnari,Francesca Asson,Solomon Saforo Addo,Elisa Orlandi,Marta Menegazzi +6 more
TL;DR: In this article , the authors investigated the effect of hyperforin (HPF) on melanoma cells in a time-dependent manner, and showed that the reduction of cell proliferation accompanied by decreased expression of cyclin D1 and A2, CDK4 and of the Rb protein phosphorylation, as assessed by immunoblots.
References
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Hallmarks of cancer: the next generation.
TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.
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Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation
TL;DR: It is proposed that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass needed to produce a new cell.
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The metabolism of tumors in the body.
TL;DR: The question of whether tumor cells in living animals can be killed off through lack of energy, and the related question of how the tumors are supplied with oxygen and glucose in the body are discussed.
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Tumor Cell Metabolism: Cancer's Achilles' Heel
TL;DR: The peculiarities of tumor cell metabolism are reviewed to discuss the alterations in signal transduction pathways and/or enzymatic machineries that account for metabolic reprogramming of transformed cells.
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Metabolic Competition in the Tumor Microenvironment Is a Driver of Cancer Progression
Chih-Hao Chang,Jing Qiu,David O’Sullivan,Michael D. Buck,Takuro Noguchi,Jonathan D. Curtis,Qiongyu Chen,Mariel Gindin,Matthew M. Gubin,Gerritje J.W. van der Windt,Elena Tonc,Robert D. Schreiber,Edward J. Pearce,Erika L. Pearce +13 more
TL;DR: It is shown that tumor-imposed metabolic restrictions can mediate T cell hyporesponsiveness during cancer, and it is found that blocking PD-L1 directly on tumors dampens glycolysis by inhibiting mTOR activity and decreasing expression of gly colysis enzymes.