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脂肪因子对肿瘤代谢的重编程作用是肥胖相关癌症进展的关键驱动因素。

Tumor Metabolic Reprogramming by Adipokines as a Critical Driver of Obesity-Associated Cancer Progression.

机构信息

College of Pharmacy, Yeungnam University, Gyeongsan 38541, Korea.

Research Institute of Cell Culture, Yeungnam University, Gyeongsan 38541, Korea.

出版信息

Int J Mol Sci. 2021 Feb 1;22(3):1444. doi: 10.3390/ijms22031444.

DOI:10.3390/ijms22031444
PMID:33535537
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7867092/
Abstract

Adiposity is associated with an increased risk of various types of carcinoma. One of the plausible mechanisms underlying the tumor-promoting role of obesity is an aberrant secretion of adipokines, a group of hormones secreted from adipose tissue, which have exhibited both oncogenic and tumor-suppressing properties in an adipokine type- and context-dependent manner. Increasing evidence has indicated that these adipose tissue-derived hormones differentially modulate cancer cell-specific metabolism. Some adipokines, such as leptin, resistin, and visfatin, which are overproduced in obesity and widely implicated in different stages of cancer, promote cellular glucose and lipid metabolism. Conversely, adiponectin, an adipokine possessing potent anti-tumor activities, is linked to a more favorable metabolic phenotype. Adipokines may also play a pivotal role under the reciprocal regulation of metabolic rewiring of cancer cells in tumor microenvironment. Given the fact that metabolic reprogramming is one of the major hallmarks of cancer, understanding the modulatory effects of adipokines on alterations in cancer cell metabolism would provide insight into the crosstalk between obesity, adipokines, and tumorigenesis. In this review, we summarize recent insights into putative roles of adipokines as mediators of cellular metabolic rewiring in obesity-associated tumors, which plays a crucial role in determining the fate of tumor cells.

摘要

肥胖与多种类型的癌的风险增加有关。肥胖促进肿瘤发生的机制之一可能是脂肪细胞因子的异常分泌,脂肪细胞因子是一组从脂肪组织分泌的激素,以脂肪因子类型和上下文依赖的方式表现出致癌和抑癌特性。越来越多的证据表明,这些脂肪组织来源的激素可差异化调节癌细胞特异性代谢。一些脂肪细胞因子,如瘦素、抵抗素和内脂素,在肥胖中过度产生,并广泛涉及癌症的不同阶段,促进细胞葡萄糖和脂质代谢。相反,脂联素是一种具有强大抗肿瘤活性的脂肪细胞因子,与更有利的代谢表型相关。脂肪细胞因子在肿瘤微环境中癌细胞代谢重编程的相互调节下也可能发挥关键作用。鉴于代谢重编程是癌症的主要标志之一,了解脂肪细胞因子对癌细胞代谢改变的调节作用将深入了解肥胖、脂肪细胞因子和肿瘤发生之间的串扰。在这篇综述中,我们总结了脂肪细胞因子作为肥胖相关肿瘤细胞代谢重编程介质的潜在作用的最新见解,这在决定肿瘤细胞的命运方面起着至关重要的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c90d/7867092/712d989c268a/ijms-22-01444-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c90d/7867092/1f8cf4821d40/ijms-22-01444-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c90d/7867092/b5900ea7f3ae/ijms-22-01444-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c90d/7867092/712d989c268a/ijms-22-01444-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c90d/7867092/1f8cf4821d40/ijms-22-01444-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c90d/7867092/b5900ea7f3ae/ijms-22-01444-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c90d/7867092/712d989c268a/ijms-22-01444-g003.jpg

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