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A VEGF-A/SOX2/SRSF2 network controls VEGFR1 pre-mRNA alternative splicing in lung carcinoma cells

Cherine Abou Faycal1,2, Sylvie Gazzeri1,2, Beatrice Eymin3,4

  • 1INSERM U1209, CNRS UMR5309, Institute For Advanced Biosciences, Grenoble, 38042, France.

Scientific Reports
|January 25, 2019
PubMed

Insights

Researchers discovered a new signaling network controlling soluble VEGFR1 (sVEGFR1-i13) expression in lung cancer. This network, involving VEGF165, SOX2, and SRSF2, is activated by anti-angiogenic therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Soluble VEGFR1 (sVEGFR1-i13) is a truncated receptor variant implicated in squamous lung carcinoma progression and anti-angiogenic therapy response.
  • Understanding the regulation of sVEGFR1-i13 is crucial for developing more effective cancer treatments.

Purpose of the Study:

  • To identify regulators of sVEGFR1-i13 expression in squamous lung carcinoma.
  • To elucidate the mechanism by which anti-angiogenic therapies influence sVEGFR1-i13 levels.

Main Methods:

  • Investigated the role of VEGF-A splice variants in regulating sVEGFR1-i13.
  • Examined the cooperation between VEGF165, SOX2, and SRSF2 in controlling sVEGFR1-i13 expression.
  • Analyzed the impact of anti-angiogenic therapies on sVEGFR1-i13 protein levels.

Main Results:

  • VEGF165, a VEGF-A splice variant, was identified as a key regulator of sVEGFR1-i13 expression.
  • VEGF165 cooperates with transcription factor SOX2 and splicing factor SRSF2 to control sVEGFR1-i13 expression.
  • Anti-angiogenic therapies up-regulate sVEGFR1-i13 protein in squamous lung carcinoma via the VEGF165/SOX2/SRSF2 network.

Conclusions:

  • A novel signaling network (VEGF165/SOX2/SRSF2) controlling VEGFR1 pre-mRNA alternative splicing in cancer cells has been identified.
  • This network plays a significant role in the response of squamous lung carcinoma to anti-angiogenic therapies.
  • Findings provide new insights into the molecular mechanisms underlying cancer progression and treatment resistance.

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