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N6-甲基腺苷诱导的ERRγ通过上调ABCB1和代谢重编程触发癌细胞的化疗耐药性。

-methyladenosine-induced ERRγ triggers chemoresistance of cancer cells through upregulation of ABCB1 and metabolic reprogramming.

作者信息

Chen Zhuojia, Wu Long, Zhou Jiawang, Lin Xinyao, Peng Yanxi, Ge Lichen, Chiang Cheng-Ming, Huang Hui, Wang Hongsheng, He Weiling

机构信息

Sun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.

Guangdong Key Laboratory of Chiral Molecule and Drug Discovery, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, Guangdong 510006, China.

出版信息

Theranostics. 2020 Feb 10;10(8):3382-3396. doi: 10.7150/thno.40144. eCollection 2020.

DOI:10.7150/thno.40144
PMID:32206097
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7069076/
Abstract

: Drug resistance severely reduces treatment efficiency of chemotherapy and leads to poor prognosis. However, regulatory factors of chemoresistant cancer cells are largely unknown. : The expression of estrogen receptor related receptors (ERRs) in chemoresistant cancer cells are checked. The roles of ERRγ in chemoresistance are confirmed by and studies. The mechanisms responsible for ERRγ-regulated expression of and are investigated. : The expression of ERRγ is upregulated in chemoresistant cancer cells. Targeted inhibition of ERRγ restores the chemosensitivity. ERRγ can directly bind to the promoter of to increase its transcription. An elevated interaction between ERRγ and p65 in chemoresistant cells further strengthens transcription of . Further, ERRγ can increase the fatty acid oxidation (FAO) in chemoresistant cells via regulation of the rate-limiting enzyme of FAO. The upregulated ERRγ in chemoresistant cancer cells might be due to increased levels of N6-methyladenosine (mA) can trigger the splicing of precursor mRNA. : mA induced ERRγ confers chemoresistance of cancer cells through upregulation of and

摘要

耐药性严重降低了化疗的治疗效果并导致预后不良。然而，化疗耐药癌细胞的调控因子在很大程度上尚不清楚。

检测化疗耐药癌细胞中雌激素受体相关受体（ERRs）的表达。通过[具体研究1]和[具体研究2]研究证实ERRγ在化疗耐药中的作用。研究ERRγ调节[相关基因1]和[相关基因2]表达的机制。

ERRγ在化疗耐药癌细胞中的表达上调。靶向抑制ERRγ可恢复化学敏感性。ERRγ可直接结合[相关基因1]的启动子以增加其转录。化疗耐药细胞中ERRγ与p65之间增强的相互作用进一步增强了[相关基因1]的转录。此外，ERRγ可通过调节脂肪酸氧化（FAO）的限速酶[相关酶]来增加化疗耐药细胞中的脂肪酸氧化。化疗耐药癌细胞中ERRγ的上调可能是由于N6-甲基腺苷（mA）水平升高可触发前体[相关mRNA]的剪接。

mA诱导的ERRγ通过上调[相关基因1]和[相关基因2]赋予癌细胞化疗耐药性

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f912/7069076/f5309bd3bb4d/thnov10p3382g008.jpg
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