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Updated: Oct 9, 2025
Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
Published on: April 26, 2017
Targeting Splicing Factor SRSF6 for Cancer Therapy
Wenting She1,2, Jun Shao3, Rong Jia1
1The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Abstract:
Aberrant alternative splicing of pre-mRNA is an emerging cancer hallmark. Many cancer-associated genes undergo alternative splicing to produce multiple isoforms with diverse or even antagonistic functions. Oncogenic isoforms are often up-regulated, whereas tumor suppressive isoforms are down-regulated during tumorigenesis. Serine/arginine-rich splicing factor 6 (SRSF6) is an important splicing factor that regulates the alternative splicing of hundreds of target genes, including many cancer-associated genes. The potential roles of SRSF6 in cancers have attracted increasing attentions in the past decade. Accumulated pieces of evidence have shown that SRSF6 is a potential oncogenic gene that promotes oncogenic splicing when overexpressed. Targeting SRSF6 may suppress tumorigenesis. In this review, we describe the gene, mRNA, and protein structure of SRSF6; summarize the current understanding of the expression, functions, and regulatory mechanisms of SRSF6 during tumorigenesis; and discuss the potential application of targeting SRSF6 in cancer treatment.
Insights
Aberrant alternative splicing is a cancer hallmark. Serine/arginine-rich splicing factor 6 (SRSF6) promotes oncogenic splicing when overexpressed, suggesting it
Area of Science:
- Molecular Biology
- Cancer Research
- Genetics
Background:
- Aberrant alternative splicing is a key feature in cancer development.
- Splicing factors regulate gene expression by controlling alternative splicing.
- Serine/arginine-rich splicing factor 6 (SRSF6) influences splicing of numerous cancer-associated genes.
Purpose of the Study:
- To review the structure, expression, and function of SRSF6 in cancer.
- To summarize the regulatory mechanisms of SRSF6 in tumorigenesis.
- To discuss SRSF6 as a potential therapeutic target in cancer treatment.
Main Methods:
- Literature review of studies on SRSF6 and cancer.
- Analysis of SRSF6 gene, mRNA, and protein structure.
- Summary of experimental evidence on SRSF6 function and regulation.
Main Results:
- SRSF6 is overexpressed in many cancers.
- SRSF6 promotes the production of oncogenic splicing isoforms.
- SRSF6 plays a significant role in promoting tumorigenesis.
Conclusions:
- SRSF6 is an oncogenic splicing factor.
- Targeting SRSF6 holds promise for cancer therapy.
- Further research into SRSF6 regulation and targeting is warranted.
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