N6-methyladenosine (m6A) in pancreatic cancer: Regulatory mechanisms and future direction

N-6-methyladenosine (m(6)A), the most abundant RNA modification in eukaryotes, plays a pivotal role in regulating many cellular and biological processes. Aberrant m(6)A modification has recently been involved in carcinogenesis in various cancers, including pancreatic cancer. Pancreatic cancer is one of the deadliest cancers. It is a heterogeneous malignant disease characterized by a plethora of diverse genetic and epigenetic events. Increasing evidence suggests that dysregulation of m(6)A regulatory factors, such as methyltransferases, demethylases, and m(6)A-binding proteins, profoundly affects the development and progression of pancreatic cancer. In addition, m(6)A regulators and m(6)A target transcripts may be promising early diagnostic and prognostic cancer biomarkers, as well as therapeutic targets. In this review, we highlight the biological functions and mechanisms of m(6)A in pancreatic cancer and discuss the potential of m(6)A modification in clinical applications.

Automated summary

N-6-methyladenosine (m(6)A), the most abundant RNA modification in eukaryotes, plays a crucial role in pancreatic cancer and dysregulation of its regulatory factors can profoundly affect the disease progression. m(6)A may serve as potential early diagnostic and therapeutic targets for pancreatic cancer.