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PTBP1 and PTBP2 impaired autoregulation of SRSF3 in cancer cells

Jihua Guo1, Jun Jia1, Rong Jia1

  • 1Hubei-MOST KLOS &KLOBME, School &Hospital of Stomatology, Wuhan University, Wuhan, 430079, PR China.

Scientific Reports
|September 30, 2015
PubMed

Insights

Overexpression of splicing factor SRSF3 in oral cancer is linked to impaired autoregulation. This impairment, caused by PTBP1/PTBP2, leads to increased SRSF3, promoting cancer progression.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • RNA Splicing

Background:

  • Splicing factors regulate gene expression through alternative splicing.
  • Overexpression of splicing factors like SRSF3 is associated with oncogenesis.
  • Mechanisms driving splicing factor overexpression in cancer are not fully understood.

Purpose of the Study:

  • To investigate the mechanisms behind SRSF3 overexpression in oral squamous cell carcinoma (OSCC).
  • To elucidate the role of autoregulation in SRSF3 expression and its disruption in cancer.

Main Methods:

  • Analysis of alternative splicing events in SRSF3 pre-mRNA.
  • Investigation of protein-RNA interactions involving SRSF3, PTBP1, and PTBP2.
  • Assessment of SRSF3 and PTBP2 expression levels in OSCC cells.

Main Results:

  • Inclusion of SRSF3 exon 4, a negative autoregulatory mechanism, is reduced in OSCC cells.
  • PTBP1 and PTBP2 bind to SRSF3 exon 4, suppressing its inclusion.
  • This suppression leads to increased full-length SRSF3 and subsequently enhances PTBP2 expression.

Conclusions:

  • Impaired SRSF3 autoregulation due to PTBP1/PTBP2 activity is a novel mechanism for SRSF3 overexpression in OSCC.
  • This aberrant splicing contributes to oncogenesis by increasing functional SRSF3 levels.
  • Targeting this pathway may offer therapeutic strategies for oral cancer.

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