Published online Jan 15, 2022. doi: 10.4251/wjgo.v14.i1.75
Peer-review started: March 17, 2021
First decision: July 27, 2021
Revised: August 11, 2021
Accepted: November 30, 2021
Article in press: November 30, 2021
Published online: January 15, 2022
Processing time: 299 Days and 20.4 Hours
Gastrointestinal (GI) cancers, including colorectal cancer, pancreatic cancer, liver cancer and gastric cancer, are severe social burdens due to high incidence and mortality rates. Bromodomain and extra-terminal (BET) proteins are epigenetic readers consisting of four conserved members (BRD2, BRD3, BRD4 and BRDT). BET family perform pivotal roles in tumorigenesis through transcriptional regulation, thereby emerging as potential therapeutic targets. BET inhibitors, disrupting the interaction between BET proteins and acetylated lysines, have been reported to suppress tumor initiation and progression in most of GI cancers. In this review, we will demonstrate how BET proteins participate in the GI cancers progression and highlight the therapeutic potential of targeting BET proteins for GI cancers treatment.
Core Tip: Bromodomain and extra-terminal (BET) inhibitors, as promising targeted agents, emerge as a new therapeutic avenue for gastrointestinal (GI) cancers. Based on preclinical evidence, BET inhibitors, alone or in combination with other therapies, were effective to suppress the progression of GI cancers.