Abstract
Splicing of mRNA precursor (pre-mRNA) is a mechanism to generate multiple mRNA isoforms from a single pre-mRNA, and it plays an essential role in a variety of biological phenomena and diseases such as cancers. Previous studies have demonstrated that cancer-specific splicing events are involved in various aspects of cancers such as proliferation, migration and response to hormones, suggesting that splicing-targeting therapy can be promising as a new strategy for cancer treatment. In this review, we focus on the splicing regulation by RNA-binding proteins including Drosophila behavior/human splicing (DBHS) family proteins, serine/arginine-rich (SR) proteins and heterogeneous nuclear ribonucleoproteins (hnRNPs) in hormone-related cancers, such as breast and prostate cancers.
Highlights
Splicing of mRNA precursors is an essential mechanism in the posttranscriptional regulation of gene expression
The 5’/3’ splice site (3’ SS) and branchpoint sequence (BPS) are required for pre-mRNA splicing, these sequences alone are often insufficient to exon/intron recognition
It was reported that histone demethylase jumonji domain containing 1A (JMJD1A) recruits hnRNPF onto the region around the 5’ side of AR exon 3B, and JMJD1A and hnRNPF support the recruitment of splicing factors including U2AF65 to the 3’ SS in front of exon 3B, which leads to the inclusion of exon 3B to produce AR-V7 [89]
Summary
Splicing of mRNA precursors (pre-mRNAs) is an essential mechanism in the posttranscriptional regulation of gene expression. Pre-mRNA splicing often generates multiple mRNA isoforms from a single pre-mRNA through different exon/intron recognition patterns, or alternative splicing, which gives rise to the diversity of protein-coding sequences and cellular proteome [3,4]. Transcripts from more than 90% of multi-exon genes undergo alternative splicing [5,6]. Recent studies have shown that pre-mRNA splicing is involved in various diseases including cancers. It has been revealed that the expressions and activities of splicing factors are different among various types of cancers, which result in distinct splicing patterns of multiple transcripts that contribute to particular disease pathophysiology, such as proliferation, migration and hormone responsiveness [8,9,10,11]. We focus on the roles of splicing factors associated with hormone-related cancers, such as breast and prostate cancers
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
