RNA Modifications in Gastrointestinal Cancer: Current Status and Future Perspectives

Abstract

Gastrointestinal (GI) cancer, referring to cancers of the digestive system such as colorectal cancer (CRC), gastric cancer (GC), and liver cancer, is a major cause of cancer-related deaths in the world. A series of genetic, epigenetic, and epitranscriptomic changes occur during the development of GI cancer. The identification of these molecular events provides potential diagnostic, prognostic, and therapeutic targets for cancer patients. RNA modification is required in the posttranscriptional regulation of RNA metabolism, including splicing, intracellular transport, degradation, and translation. RNA modifications such as N6-methyladenosine (m6A) and N1-methyladenosine (m1A) are dynamically regulated by three different types of regulators named methyltransferases (writers), RNA binding proteins (readers), and demethylases (erasers). Recent studies have pointed out that abnormal RNA modification contributes to GI tumorigenesis and progression. In this review, we summarize the latest findings on the functional significance of RNA modification in GI cancer and discuss the therapeutic potential of epitranscriptomic inhibitors for cancer treatment.

The regulatory role of N6-methyladenosine RNA modification in gastric cancer: Molecular mechanisms and potential therapeutic targets

“…Immune cells in the tumor microenvironment (TME) play a key role in tumor progression, immune escape, and their impact on immunotherapeutic response. Immune checkpoint block (ICB) therapy eliminates cancer cells by targeting programmed death molecule 1 and its ligand (PD-1/PD-L1) in cytotoxic T cells and activating the immune system ( 168 ). M 6 A modification is related to PD1/PD-L1 immunotherapy.…”

N6-methyladenosine modification of B7-H3 mRNA promotes the development and progression of colorectal cancer

“… 9 Emerging evidence suggests that abnormal m6A modifications and related regulatory proteins play critical roles in cancer occurrence and development. 10 The fate of m6A-modified RNA is largely determined by the recognition of different m6A readers. 11 YTH N6-methyladenosine RNA-binding protein 1 (YTHDF1), one of the most abundant m6A readers, functionally binds to m6A-modified mRNA and accelerates target proteins translation.…”