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Androgen receptor promotes renal cell carcinoma (RCC) vasculogenic mimicry (VM) via altering TWIST1 nonsense-mediated

Bosen You1,2,3, Yin Sun3, Jie Luo3

  • 1Department of Urology, The 4th Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.

Oncogene
|January 29, 2021
PubMed

Insights

Androgen receptor (AR) promotes clear cell renal cell carcinoma (ccRCC) progression by enhancing vasculogenic mimicry (VM) through the lncRNA-TANAR/TWIST1 pathway. Targeting this AR/TANAR/TWIST1 signaling offers a potential new therapy for ccRCC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • The role of the androgen receptor (AR) in clear cell renal cell carcinoma (ccRCC) progression is known, but its specific impact on vasculogenic mimicry (VM) remains unclear.
  • Vasculogenic mimicry (VM) is a process where tumor cells form vascular-like structures, contributing to tumor growth and metastasis in various cancers, including ccRCC.

Purpose of the Study:

  • To investigate the influence of the androgen receptor (AR) on vasculogenic mimicry (VM) in clear cell renal cell carcinoma (ccRCC).
  • To elucidate the molecular mechanisms by which AR affects VM and ccRCC progression.
  • To explore the potential of targeting the AR/TANAR/TWIST1 signaling pathway for ccRCC therapy.

Main Methods:

  • Correlation analysis between AR expression and tumor-originated vasculogenesis in ccRCC patients.
  • In vitro studies using ccRCC cell lines to assess AR's effect on VM formation.
  • Mechanistic studies involving AR binding to androgen response elements (AREs) and lncRNA-TANAR expression.
  • Investigation of TANAR's interaction with TWIST1 mRNA and its effect on nonsense-mediated mRNA decay (NMD).
  • In vivo preclinical studies using mouse models with orthotopic ccRCC xenografts.

Main Results:

  • Elevated AR expression positively correlated with tumor-originated vasculogenesis in ccRCC patients.
  • AR was found to promote VM formation in ccRCC cell lines by modulating lncRNA-TANAR/TWIST1 signaling.
  • AR directly binds to AREs in the promoter region of lncRNA-TANAR, increasing its expression.
  • lncRNA-TANAR interacts with TWIST1 mRNA, inhibiting its nonsense-mediated mRNA decay (NMD).
  • In vivo studies confirmed the in vitro findings regarding the AR/TANAR/TWIST1 pathway's role in ccRCC.

Conclusions:

  • The AR/TANAR/TWIST1 signaling pathway plays a critical role in ccRCC VM formation and metastasis.
  • Targeting this newly identified AR-mediated pathway presents a potential novel anti-angiogenesis therapeutic strategy for ccRCC.
  • Understanding this mechanism could lead to improved therapies to suppress ccRCC progression.

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