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T-type calcium channels drive the proliferation of androgen-receptor negative prostate cancer cells

Roberto Silvestri1,2, Perla Pucci1, Erik Venalainen3

  • 1School of Life Health and Chemical Sciences, The Open University, Milton Keynes, UK.

The Prostate
|July 24, 2019
PubMed
Abstract

Insights

T-type calcium channels (TTCCs) are upregulated in advanced prostate cancer (PCa) and linked to poorer prognosis. Inhibiting TTCCs reduced PCa cell proliferation and survival, suggesting TTCCs as potential therapeutic targets for advanced PCa.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Androgen deprivation therapy (ADT) is standard for metastatic prostate cancer (PCa).
  • Prostate cancer can evolve into incurable castration-resistant (CRPC) or neuroendocrine (NEPC) forms after ADT.
  • The role of T-type calcium channels (TTCCs) in PCa progression remains unexplored.

Purpose of the Study:

  • To investigate the expression, copy number variants (CNV), and prognostic significance of TTCCs in prostate cancer.
  • To evaluate the effect of TTCC inhibition on prostate cancer cell proliferation and survival.

Main Methods:

  • Analysis of TTCC expression and CNV in clinical PCa datasets (Oncomine, cBioPortal).
  • Assessment of TTCC expression in PCa cell lines.
  • Inhibition of TTCCs using pharmacological agents and small interfering RNA (siRNA).
  • Measurement of cell proliferation (MTT assay) and survival (caspase assay).

Main Results:

  • TTCCs were upregulated in PCa with androgen receptor (AR) mutations.
  • Higher CNV rates correlated with PCa progression.
  • Elevated expression of the TTCC isoform CACNA1G predicted worse outcomes in early-stage PCa.
  • TTCC inhibition decreased PC-3 cell proliferation and survival.

Conclusions:

  • TTCCs are overexpressed in advanced PCa and associated with poor prognosis.
  • Inhibition of TTCCs demonstrates potential therapeutic value in advanced PCa by reducing cell proliferation and survival.
Keywords:
CACNA1GMTT assayNEPCPCaTTCC

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