Abstract
Cancer drug resistance has always been a major difficulty in cancer therapy. In the face of drug pressure, resistant cancer cells show complex molecular mechanisms including epigenetic changes to maintain survival. Studies prove that cancer cells exhibit abnormal m6A modification after acquiring drug resistance. m6A modification in the target RNA including non-coding RNA can be a controller to determine the fate and metabolism of RNA by regulating their stability, subcellular localization, or translation. In particular, m6A-modified non-coding RNA plays multiple roles in multiple drug-resistant cancer cells, which can be a target for cancer drug resistance. Here, we provide an overview of the complex regulatory mechanisms of m6A-modified non-coding RNA in cancer drug resistance, and we discuss its potential value and challenges in clinical applications.
Highlights
RNA modification determines cell fate by regulating gene expression and responds to environmental pressures [1, 2]. m6A methylation is the most common modification in mammalian RNAs
We focused on the important role of m6A modification in cancer drug resistance, summarized the molecular mechanism of m6A-modified RNA including noncoding RNA involved in cancer drug resistance, and discussed the application and clinical value of m6A modification in the prediction and treatment of cancer resistance
We summarized the research progress of m6A modification in cancer drug resistance
Summary
RNA modification determines cell fate by regulating gene expression and responds to environmental pressures [1, 2]. m6A methylation is the most common modification in mammalian RNAs. No change of global m6A levels in ovarian cancer resistant cells might be due to downregulated FTO, ALKBH5, METTL3, and METTL14. A high m6A level in 3′UTR region of the FZD10 mRNA due to the decrease of FTO and ALKBH5 was found to activate the Wnt signaling pathway, leading to PARPi resistance [57] These evidence indicated that the global m6A level is very complicated under different types of tumor cells and different therapy resistance. This complexity is due to the abnormal expression of different m6A regulators under resistant conditions. The global m6A level was regulated at different layers by “writers,” “erasers,” and “readers,” which showed irregular expression and played important roles in drug resistance of multiple cancers (Table 1). Low METTL3 expression was found in human sorafenib-resistant
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
