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The RNA-binding protein SRSF1 is a key cell cycle regulator via stabilizing NEAT1 in glioma

Xuexia Zhou1, Xuebing Li2, Lin Yu3

  • 1Department of Neuropathology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China; Tianjin Key Laboratory of Injuries, Variations and Regeneration of the Nervous System, Tianjin, China; Key Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous System, Ministry of Education, Tianjin, China.

The International Journal of Biochemistry & Cell Biology
|June 15, 2019
PubMed

Insights

Serine/arginine-rich splicing factor 1 (SRSF1) regulates glioma progression independently of splicing. SRSF1 stabilizes nuclear paraspeckle assembly transcript1 (NEAT1), a long non-coding RNA crucial for cell cycle control in glioma.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • RNA Biology

Background:

  • RNA processing is increasingly implicated in various diseases.
  • Serine/arginine-rich splicing factor 1 (SRSF1) was previously identified as an oncodriver in glioma through splicing control.
  • The splicing-independent roles of SRSF1 in glioma remain poorly understood.

Purpose of the Study:

  • To investigate the splicing-independent mechanisms of SRSF1 in glioma.
  • To identify novel targets and pathways regulated by SRSF1 in glioma.
  • To explore the therapeutic potential of SRSF1 and its targets in glioma.

Main Methods:

  • Integrated data mining of SRSF1-co-expressed and SRSF1-affected genes.
  • Experimental validation of SRSF1-NEAT1 interaction and functional effects.
  • Analysis of SRSF1 and NEAT1 expression correlation in cancer datasets.

Main Results:

  • SRSF1 is highly expressed across multiple tumor types and acts as a crucial cell cycle regulator in glioma.
  • Nuclear paraspeckle assembly transcript1 (NEAT1), a long non-coding RNA (lncRNA), was identified as a direct target of SRSF1.
  • SRSF1 binds to NEAT1, enhancing its RNA stability and consequently retarding glioma cell cycle progression, similar to SRSF1 knockdown effects.

Conclusions:

  • SRSF1 exerts splicing-independent functions in glioma by stabilizing NEAT1, a lncRNA that regulates the cell cycle.
  • The SRSF1-NEAT1 axis plays a significant role in gliomagenesis.
  • Both SRSF1 and NEAT1 represent promising therapeutic targets for glioma treatment.
Keywords:
Cell cycle progressionGliomaNEAT1RNA stabilitySRSF1

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