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Biological function and molecular mechanism of SRSF3 in cancer and beyond
Jian Xiong1, Yinshuang Chen2, Weipeng Wang2
1Institute of Medical Biotechnology, Suzhou Vocational Health College, Suzhou, Jiangsu 215009, P.R. China.
Abstract:
Serine/arginine-rich splicing factor 3 (SRSF3; also known as SRp20), an important member of the family of SRSFs, is abnormally expressed in tumors, resulting in aberrant splicing of hub genes, such as CD44, HER2, MDM4, Rac family small GTPase 1 and tumor protein p53. Under normal conditions, the splicing and expression of SRSF3 are strictly regulated. However, the splicing, expression and phosphorylation of SRSF3 are abnormal in tumors. SRSF3 plays important roles in the occurrence and development of tumors, including the promotion of tumorigenesis, cellular proliferation, the cell cycle and metastasis, as well as inhibition of cell senescence, apoptosis and autophagy. SRSF3-knockdown significantly inhibits the proliferation and metastatic characteristics of tumor cells. Therefore, SRSF3 may be suggested as a novel anti-tumor target. The other biological functions of SRSF3 and its regulatory mechanisms are also summarized in the current review.
Insights
Serine/arginine-rich splicing factor 3 (SRSF3) is abnormally expressed in tumors, driving cancer progression. Inhibiting SRSF3 suppresses tumor cell proliferation and metastasis, suggesting it as a potential anti-tumor target.
Area of Science:
- Molecular Biology
- Cancer Biology
- Gene Regulation
Background:
- Serine/arginine-rich splicing factor 3 (SRSF3), also known as SRp20, is a key splicing factor.
- SRSF3 expression and splicing are tightly regulated under normal physiological conditions.
- Aberrant SRSF3 expression is observed in various tumors.
Purpose of the Study:
- To review the biological functions of SRSF3 in cancer.
- To explore the regulatory mechanisms of SRSF3.
- To evaluate SRSF3 as a potential anti-tumor therapeutic target.
Main Methods:
- Literature review of studies on SRSF3 in cancer.
- Analysis of SRSF3's role in splicing of key cancer-related genes (e.g., CD44, HER2, MDM4, p53).
- Examination of SRSF3's impact on tumor cell proliferation, cell cycle, metastasis, senescence, apoptosis, and autophagy.
Main Results:
- SRSF3 dysregulation contributes to aberrant splicing of critical genes in tumors.
- SRSF3 promotes tumorigenesis, proliferation, cell cycle progression, and metastasis.
- SRSF3 inhibits cell senescence, apoptosis, and autophagy.
- SRSF3 knockdown significantly impairs tumor cell proliferation and metastasis.
Conclusions:
- SRSF3 plays a multifaceted role in cancer development and progression.
- Dysregulated SRSF3 impacts multiple hallmarks of cancer.
- SRSF3 represents a promising novel target for anti-cancer therapies.
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