4.6 Review

Role of HIF-1α/ERRα in Enhancing Cancer Cell Metabolism and Promoting Resistance of Endometrial Cancer Cells to Pyroptosis

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FRONTIERS IN ONCOLOGY
卷 12, 期 -, 页码 -

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FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2022.881252

关键词

glucose metabolism; lipid metabolism; HIF-1 alpha; ERR alpha; endometrial cancer

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资金

  1. Natural Science Foundation of Fujian Province
  2. Joint Funds for the Innovation of Science and Technology, Fujian Province [2020J02059, 2021J01404]
  3. [2020Y9160]

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Oxygen is crucial for energy metabolism in tumors, which often occur in a hypoxic microenvironment. The interaction between HIF-1 alpha and ERR alpha plays a key role in regulating the metabolic and functional changes in cancer cells. This review gives an overview of the tumor metabolic reprogramming involving HIF-1 alpha/ERR alpha and explores their role in promoting tumor growth adaptation and pyroptosis resistance.
Oxygen is critical to energy metabolism, and tumors are often characterized by a hypoxic microenvironment. Owing to the high metabolic energy demand of malignant tumor cells, their survival is promoted by metabolic reprogramming in the hypoxic microenvironment, which can confer tumor cell resistance to pyroptosis. Pyroptosis resistance can inhibit anti-tumor immunity and promote the development of malignant tumors. Hypoxia inducible factor-1 alpha (HIF-1 alpha) is a key regulator of metabolic reprogramming in tumor cells, and estrogen-related receptor alpha (ERR alpha) plays a key role in regulating cellular energy metabolism. Therefore, the close interaction between HIF-1 alpha and ERR alpha influences the metabolic and functional changes in cancer cells. In this review, we summarize the reprogramming of tumor metabolism involving HIF-1 alpha/ERR alpha. We review our understanding of the role of HIF-1 alpha/ERR alpha in promoting tumor growth adaptation and pyroptosis resistance, emphasize its key role in energy homeostasis, and explore the regulation of HIF-1 alpha/ERR alpha in preventing and/or treating endometrial carcinoma patients. This review provides a new perspective for the study of the molecular mechanisms of metabolic changes in tumor progression.

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