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RASAL2 inhibits tumor angiogenesis via p-AKT/ETS1 signaling in bladder cancer

Ke Hui1, Shiqi Wu1, Yangyang Yue1

  • 1Department of Urology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, PR China.

Cellular Signalling
|April 28, 2018
PubMed

Insights

RASAL2 inhibits bladder cancer (BCa) angiogenesis by regulating AKT, ETS1, and VEGFA pathways. This discovery identifies RASAL2 as a potential therapeutic target for advanced BCa.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Muscle-invasive or metastatic bladder cancer (BCa) poses a significant threat to patients.
  • Tumor angiogenesis is critical for BCa progression, but its mechanisms remain unclear.
  • Understanding the molecular drivers of BCa angiogenesis is essential for developing new therapies.

Purpose of the Study:

  • To investigate the role of RASAL2 in bladder cancer (BCa) angiogenesis.
  • To elucidate the molecular mechanisms by which RASAL2 affects BCa progression.
  • To identify potential therapeutic targets for advanced BCa.

Main Methods:

  • Utilized shRNA/siRNA knockdown and ectopic cDNA expression of RASAL2 in BCa models.
  • Assessed the impact of RASAL2 modulation on angiogenesis-related signaling pathways (e.g., AKT phosphorylation).
  • Examined the expression levels of key angiogenesis factors (ETS1, VEGFA, CD31) in vitro and in vivo.
  • Correlated RASAL2 expression with VEGFA and CD31 levels in human BCa tissues and xenografts.

Main Results:

  • RASAL2 was identified as an inhibitor of bladder cancer (BCa) angiogenesis.
  • RASAL2 downregulation led to increased AKT phosphorylation, subsequently upregulating ETS1 and VEGFA expression.
  • A negative correlation was observed between RASAL2 expression and VEGFA or CD31 levels in BCa specimens.

Conclusions:

  • RASAL2 plays a crucial inhibitory role in bladder cancer (BCa) angiogenesis.
  • The study reveals a novel molecular mechanism involving RASAL2, AKT, ETS1, and VEGFA in BCa progression.
  • RASAL2 represents a promising new therapeutic target for treating muscle-invasive or metastatic bladder cancer.
Keywords:
AKT/ETS1 signalingAngiogenesisBladder cancerRASAL2VEGFA

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