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Updated: Dec 24, 2025

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
Published on: April 26, 2017
Aberrant expression and regulatory network of splicing factor-SRSF3 in tumors
1Institute of Chronic Disease, Qingdao Municipal Hospital, Qingdao University, Qingdao 266000, China.
Abstract:
Alternative splicing facilitates the splicing of precursor RNA into different isoforms. Alternatively spliced transcripts often exhibit antagonistic functions or differential temporal or spatial expression patterns. There is increasing evidence that alternative splicing, especially by the serine-arginine rich (SR) protein family, leads to abnormal expression patterns and is closely related to the development of cancer. SRSF3, also known as SRp20, is a splicing factor. Through alternative splicing, it plays important roles in regulating various biological functions, such as cell cycle, cell proliferation, migration and invasion, under pathological and physiological conditions. Deregulation of SRSF3 is an essential feature of cancers. SRSF3 is also considered a candidate therapeutic target. Therefore, the involvement of abnormal splicing in tumorigenesis and the regulation of splicing factors deserve further analysis and discussion. Here, we summarize the function of SRSF3-regulated alternative transcripts in cancer cell biology at different stages of tumor development and the regulation of SRSF3 in tumorigenesis.
Insights
Alternative splicing, regulated by serine-arginine rich (SR) proteins like SRSF3 (SRp20), is crucial in cancer development. This review explores SRSF3
Area of Science:
- Molecular Biology
- Cancer Research
- RNA Splicing
Background:
- Alternative splicing generates diverse RNA isoforms with varied functions.
- Aberrant splicing, particularly by SR proteins, is linked to cancer development.
- SRSF3 (SRp20) is a key splicing factor implicated in numerous cellular processes.
Purpose of the Study:
- To summarize the role of SRSF3-regulated alternative splicing in cancer cell biology.
- To discuss the regulation of SRSF3 in tumorigenesis.
- To highlight SRSF3 as a potential therapeutic target in cancer.
Main Methods:
- Review of existing literature on SRSF3 function and alternative splicing in cancer.
- Analysis of SRSF3's impact on cancer cell proliferation, migration, and invasion.
- Discussion of SRSF3's regulatory mechanisms in tumor development.
Main Results:
- SRSF3 deregulation is a hallmark of many cancers.
- SRSF3-mediated alternative splicing influences critical cancer cell behaviors.
- SRSF3 plays significant roles across different stages of tumor progression.
Conclusions:
- SRSF3 is a critical regulator of alternative splicing in cancer.
- Understanding SRSF3's role in tumorigenesis is essential for developing targeted therapies.
- SRSF3 represents a promising therapeutic target for various cancers.
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