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Splicing factors: Insights into their regulatory network in alternative splicing in cancer
- Source :
- Cancer letters. 501
- Publication Year :
- 2020
-
Abstract
- More than 95% of all human genes are alternatively spliced after transcription, which enriches the diversity of proteins and regulates transcript and/or protein levels. The splicing isoforms produced from the same gene can manifest distinctly, even exerting opposite effects. Mounting evidence indicates that the alternative splicing (AS) mechanism is ubiquitous in various cancers and drives the generation and maintenance of various hallmarks of cancer, such as enhanced proliferation, inhibited apoptosis, invasion and metastasis, and angiogenesis. Splicing factors (SFs) play pivotal roles in the recognition of splice sites and the assembly of spliceosomes during AS. In this review, we mainly discuss the similarities and differences of SF domains, the details of SF function in AS, the effect of SF-driven pathological AS on different hallmarks of cancer, and the main drivers of SF expression level and subcellular localization. In addition, we briefly introduce the application prospects of targeted therapeutic strategies, including small-molecule inhibitors, siRNAs and splice-switching oligonucleotides (SSOs), from three perspectives (drivers, SFs and pathological AS). Finally, we share our insights into the potential direction of research on SF-centric AS-related regulatory networks.
- Subjects :
- 0301 basic medicine
Gene isoform
Cancer Research
Spliceosome
Alternative splicing
Computational biology
Biology
Post-transcriptional modification
03 medical and health sciences
Alternative Splicing
030104 developmental biology
0302 clinical medicine
Oncology
Transcription (biology)
030220 oncology & carcinogenesis
Neoplasms
RNA splicing
Animals
Humans
Human genome
Gene Regulatory Networks
RNA Splicing Factors
Gene
Subjects
Details
- ISSN :
- 18727980
- Volume :
- 501
- Database :
- OpenAIRE
- Journal :
- Cancer letters
- Accession number :
- edsair.doi.dedup.....0a995037a4f4677e2ef921bfe9371d9b