Abstract
m6A RNA methylation, which serves as a critical regulator of transcript expression, has gathered tremendous scientific interest in recent years. From RNA processing to nuclear export, RNA translation to decay, m6A modification has been studied to affect various aspects of RNA metabolism, and it is now considered as one of the most abundant epitranscriptomic modification. RNA methyltransferases (writer), m6A-binding proteins (readers), and demethylases (erasers) proteins are frequently upregulated in several neoplasms, thereby regulating oncoprotein expression, augmenting tumor initiation, enhancing cancer cell proliferation, progression, and metastasis. Though the potential role of m6A methylation in growth and proliferation of cancer cells has been well documented, its potential role in development of therapy resistance in cancer is not clear. In this review, we focus on m6A-associated regulation, mechanisms, and functions in acquired chemoresistance, radioresistance, and resistance to immunotherapy in cancer.
Highlights
Cancer remains a key public health concern posing a major threat to the world’s population
Methylated RNA immunoprecipitation (Me-RIP) study suggests that TRIM11 m6A level was higher in cisplatin resistant cells compared to sensitive cells in nasopharyngeal carcinoma (NPC) lines
We found that alkB homolog 5 (ALKBH5) is directly regulated by human RNA helicase DDX3, which leads to decreased m6A methylation in FOXM1 and NANOG nascent transcript that contribute to cisplatin resistance in OSCC [31]
Summary
Cancer remains a key public health concern posing a major threat to the world’s population. The chemoresistant phenotype of cancer cells can be attributed due to impaired apoptosis, altered cellular metabolism, decreased drug accumulation, reduced drug-target interactions, and increased populations of cancer stem cells [2]. These are the endpoint events and the causative factors responsible for acquired chemoresistance is yet to be known. YT521-B homology(YTH) proteins, insulin-like growth factor 2 mRNA binding proteins (IGF2BPs), eukaryotic initiation factor 3 (eIF3), heterogeneous nuclear ribonucleoproteins (HNRNPs), and fragile X mental retardation proteins (FMRPs) are included under “reader” complex that recognizes the m6A RNA modification and initiates downstream signaling [13]. We have focused on the mechanisms of RNA m6A modification-associated therapy resistance and possible approaches to overcome it
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