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癌症干细胞的代谢异质性与灵活性

The Metabolic Heterogeneity and Flexibility of Cancer Stem Cells.

作者信息

Tanabe Atsushi, Sahara Hiroeki

机构信息

Laboratory of Biology Azabu University School of Veterinary Medicine 1-17-71 Fuchinobe, Chuo-ku, Sagamihara, Kanagawa 252-5201, Japan.

出版信息

Cancers (Basel). 2020 Sep 28;12(10):2780. doi: 10.3390/cancers12102780.

DOI:10.3390/cancers12102780
PMID:32998263
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7601708/
Abstract

Numerous findings have indicated that CSCs, which are present at a low frequency inside primary tumors, are the main cause of therapy resistance and cancer recurrence. Although various therapeutic methods targeting CSCs have been attempted for eliminating cancer cells completely, the complicated characteristics of CSCs have hampered such attempts. In analyzing the biological properties of CSCs, it was revealed that CSCs have a peculiar metabolism that is distinct from non-CSCs to maintain their stemness properties. The CSC metabolism involves not only the catabolic and anabolic pathways, but also intracellular signaling, gene expression, and redox balance. In addition, CSCs can reprogram their metabolism to flexibly respond to environmental changes. In this review, we focus on the flexible metabolic mechanisms of CSCs, and highlight the new therapeutics that target CSC metabolism.

摘要

众多研究结果表明,癌症干细胞(CSCs)在原发性肿瘤中所占比例较低,却是治疗耐药性和癌症复发的主要原因。尽管已经尝试了各种针对癌症干细胞的治疗方法以彻底消除癌细胞,但癌症干细胞的复杂特性阻碍了这些尝试。在分析癌症干细胞的生物学特性时发现,癌症干细胞具有一种独特的代谢方式,与非癌症干细胞不同,以维持其干性特征。癌症干细胞的代谢不仅涉及分解代谢和合成代谢途径,还包括细胞内信号传导、基因表达和氧化还原平衡。此外,癌症干细胞可以重新编程其代谢,以灵活应对环境变化。在本综述中,我们重点关注癌症干细胞灵活的代谢机制,并强调针对癌症干细胞代谢的新疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f047/7601708/bdb84ed2b2fb/cancers-12-02780-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f047/7601708/2c84e413abfd/cancers-12-02780-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f047/7601708/3e82c814b203/cancers-12-02780-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f047/7601708/c3a2f6e9907c/cancers-12-02780-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f047/7601708/bdb84ed2b2fb/cancers-12-02780-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f047/7601708/2c84e413abfd/cancers-12-02780-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f047/7601708/3e82c814b203/cancers-12-02780-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f047/7601708/c3a2f6e9907c/cancers-12-02780-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f047/7601708/bdb84ed2b2fb/cancers-12-02780-g004.jpg

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DAZAP1 maintains gastric cancer stemness by inducing mitophagy.DAZAP1通过诱导线粒体自噬维持胃癌干性。
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