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Adipokines as Regulators of Autophagy in Obesity-Linked Cancer

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CELLS
卷 11, 期 20, 页码 -

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MDPI
DOI: 10.3390/cells11203230

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adipokines; autophagy; cancer; obesity; leptin; adiponectin; resistin; apelin; visfatin

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Excess body weight and obesity have been identified as significant risk factors for cancer development, with adipokines playing a crucial role in promoting an inflammatory microenvironment conducive to carcinogenesis and tumor progression. Autophagy, a process implicated in both tumor suppression and cancer progression, has been suggested as a therapeutic target in cancer treatment, with its effectiveness potentially influenced by tumor type and microenvironmental conditions influenced by circulating adipokines.
Excess body weight and obesity have become significant risk factors for cancer development. During obesity, adipose tissue alters its biological function, deregulating the secretion of bioactive factors such as hormones, cytokines, and adipokines that promote an inflammatory microenvironment conducive to carcinogenesis and tumor progression. Adipokines regulate tumor processes such as apoptosis, proliferation, migration, angiogenesis, and invasion. Additionally, it has been found that they can modulate autophagy, a process implicated in tumor suppression in healthy tissue and cancer progression in established tumors. Since the tumor-promoting role of autophagy has been well described, the process has been suggested as a therapeutic target in cancer. However, the effects of targeting autophagy might depend on the tumor type and microenvironmental conditions, where circulating adipokines could influence the role of autophagy in cancer. Here, we review recent evidence related to the role of adipokines in cancer cell autophagy in an effort to understand the tumor response in the context of obesity under the assumption of an autophagy-targeting treatment.

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