The Role of m(6)A Modification and m(6)A Regulators in Esophageal Cancer

SIMPLE SUMMARY: N(6)-methyladenosine (m(6)A) modification and m(6)A regulators play important roles in the occurrence and development of various cancers. Esophageal cancer (ESCA), one of the most common gastrointestinal tumors, seriously affects people’s health. In this review article, we summarized the role and possible mechanism of m(6)A modification and m(6)A regulators in the occurrence, progression, remedy and prognosis of ESCA, which might be useful for determining the pathogenesis of ESCA and providing direction for the future research of ESCA. ABSTRACT: N(6)-methyladenosine (m(6)A) modification, the most prevalent RNA modification, is involved in all aspects of RNA metabolism, including RNA processing, nuclear export, stability, translation and degradation. Therefore, m(6)A modification can participate in various physiological functions, such as tissue development, heat shock response, DNA damage response, circadian clock control and even in carcinogenesis through regulating the expression or structure of the gene. The deposition, removal and recognition of m(6)A are carried out by methyltransferases, demethylases and m(6)A RNA binding proteins, respectively. Aberrant m(6)A modification and the dysregulation of m(6)A regulators play critical roles in the occurrence and development of various cancers. The pathogenesis of esophageal cancer (ESCA) remains unclear and the five-year survival rate of advanced ESCA patients is still dismal. Here, we systematically reviewed the recent studies of m(6)A modification and m(6)A regulators in ESCA and comprehensively analyzed the role and possible mechanism of m(6)A modification and m(6)A regulators in the occurrence, progression, remedy and prognosis of ESCA. Defining the effect of m(6)A modification and m(6)A regulators in ESCA might be helpful for determining the pathogenesis of ESCA and providing some ideas for an early diagnosis, individualized treatment and improved prognosis of ESCA patients.