N6-methyladenosine (m6A) as a regulator of carcinogenesis and drug resistance by targeting epithelial-mesenchymal transition and cancer stem cells

被引:9
|
作者
Wang, Chuhan [1 ,2 ]
Ma, Danli [1 ]
Yu, Huimin [1 ]
Zhuo, Zhihong [1 ]
Ye, Zhiying [1 ]
机构
[1] Univ Chinese Acad Sci, Hwa Mei Hosp, Dept Gynecol, 31500, Ningbo, Zhejiang, Peoples R China
[2] Med Sch NingBo Univ, 31500, Ningbo, Zhejiang, Peoples R China
关键词
m6A; Carcinogenesis; Drug resistance; Epithelial-mesenchymal transition; Cancer stem cells; M(6)A RNA METHYLATION; MESSENGER-RNA; NUCLEAR-RNA; CISPLATIN RESISTANCE; MOLECULAR-MECHANISMS; N-6-METHYLADENOSINE; DEMETHYLASE; EXPRESSION; ALKBH5; FTO;
D O I
10.1016/j.heliyon.2023.e14001
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Emergence of drug resistance to chemotherapeutic agents is the principal obstacle towards curative cancer treatment in human cancer patients. It is in an urgent to explore the underlying molecular mechanisms to overcome the drug resistance. N6-Methyladenosine (m6A) RNA modification is the most abundant reversible RNA modification and has emerged in recent years to regulate gene expression in eukaryotes. Recent evidence has identified m6A is associated with cancer pathogenesis and drug resistance, contributing to the self-renewal and differentiation of cancer stem cell, tumor epithelial-mesenchymal transition (EMT) and tumor metastasis. Here we reviewed up-to-date knowledge of the relationship between m6A modulation and drug resistance. Furthermore, we illustrated the underlying mechanisms of m6A modulation in drug resistance. Lastly, we discussed the regulation of m6A modulation in EMT and cancer stem cells. Hence, it will help to provide significant therapeutic strategies to overcome drug resistance for cancer patients by changing m6A-related proteins via targeting cancer stem cells and EMT-phenotypic cells.
引用
收藏
页数:12
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