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Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis
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SRSF5 functions as a novel oncogenic splicing factor and is upregulated by oncogene SRSF3 in oral squamous cell

Sisi Yang1, Rong Jia1, Zhuan Bian1

  • 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, PR China.

Biochimica Et Biophysica Acta. Molecular Cell Research
|June 2, 2018
PubMed

Insights

Serine/arginine-rich splicing factor 5 (SRSF5) is a novel oncogene overexpressed in oral squamous cell carcinoma (OSCC). SRSF3 promotes SRSF5 overexpression, driving OSCC cell proliferation and tumor formation.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • RNA Splicing

Background:

  • Alternative splicing of precursor messenger RNA is increasingly linked to tumorigenesis.
  • The serine/arginine-rich protein (SR) family regulates pre-mRNA alternative splicing and is implicated in cancer.
  • The specific roles of SR proteins in tumorigenesis are not fully understood.

Purpose of the Study:

  • To investigate the role of serine/arginine-rich splicing factor 5 (SRSF5) in oral squamous cell carcinoma (OSCC).
  • To elucidate the regulatory mechanism of SRSF5 expression in cancer cells.
  • To identify upstream regulators of SRSF5 in OSCC.

Main Methods:

  • Analysis of SRSF5 expression in OSCC tissues and cells.
  • Functional assays including cell proliferation, cell cycle progression, and tumor formation in nude mice.
  • Investigation of the autoregulation mechanism of SRSF5.
  • Examination of the regulatory relationship between SRSF3 and SRSF5.

Main Results:

  • SRSF5 is overexpressed in OSCC tissues and cells and promotes OSCC cell proliferation and tumor formation.
  • Overexpression of SRSF5 transformed rodent fibroblasts into tumor-forming cells.
  • Downregulation of SRSF5 inhibited oral cancer cell growth, cell cycle progression, and tumor growth.
  • SRSF5 expression is controlled by an autoregulation mechanism.
  • SRSF3, an identified oncogene, targets SRSF5, impairs its autoregulation, and promotes its overexpression in cancer cells.

Conclusions:

  • SRSF5 is a novel oncogenic splicing factor crucial for OSCC progression.
  • SRSF3 upregulates SRSF5 in OSCC cells, contributing to tumorigenesis.
  • Targeting the SRSF3-SRSF5 axis presents a potential therapeutic strategy for OSCC.
Keywords:
Alternative splicingAutoregulationOncogeneSRSF3SRSF5

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