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Androgen receptor (AR) suppresses miRNA-145 to promote renal cell carcinoma (RCC) progression independent of VHL

Yuan Chen1,2, Yin Sun2, Qun Rao3,2

  • 1Sex Hormone Research Center, Department of Urology, Tongji Medical College/Hospital, Huazhong University of Science and Technology, Wuhan, China.

Oncotarget
|August 26, 2015
PubMed

Insights

Researchers discovered a new pathway involving androgen receptor (AR) and miRNA-145 that drives renal cell carcinoma (RCC) progression. Targeting this AR-suppressed miRNA-145 pathway offers a promising therapeutic strategy for RCC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Mutational inactivation of the VHL tumor suppressor is crucial in renal cell carcinoma (RCC) development.
  • VEGF induction, mediated by VHL mutations, is a primary target in current RCC therapies.

Purpose of the Study:

  • To identify and characterize a novel signaling pathway involving androgen receptor (AR) and miRNA-145 for VEGF induction in RCC.
  • To explore the therapeutic potential of targeting this AR/miRNA-145 pathway to suppress RCC progression.

Main Methods:

  • Investigated the mechanism of AR-mediated regulation of miRNA-145 expression.
  • Utilized AR-shRNA and miRNA-145 mimics to assess their effects on RCC progression.
  • Evaluated the efficacy of miRNA-145 mimic in a preclinical RCC orthotopic xenograft mouse model.

Main Results:

  • Identified a pathway where AR suppresses miRNA-145, leading to increased expression of HIF2α/VEGF/MMP9/CCND1.
  • AR suppression or miRNA-145 mimic introduction attenuated RCC progression, irrespective of VHL status.
  • MiRNA-145 mimic demonstrated efficacy in suppressing RCC progression in a mouse model.

Conclusions:

  • AR-suppressed miRNA-145 signaling is a key driver of RCC progression by regulating HIF2α/VEGF/MMP9/CCND1.
  • Inhibition of AR or augmentation of miRNA-145 presents a promising therapeutic strategy for RCC.
Keywords:
HIF2αandrogen receptormicroRNA-145renal cell carcinoma

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