High glucose induces N-linked glycosylation-mediated functional upregulation and overexpression of Cav3.2 T-type calcium channels in neuroendocrine-like differentiated human prostate cancer cells

J Pharmacol Sci. 2017 Jan;133(1):57-60. doi: 10.1016/j.jphs.2016.12.004. Epub 2017 Jan 3.

Abstract

Given that Cav3.2 T-type Ca2+ channels were functionally regulated by asparagine (N)-linked glycosylation, we examined effects of high glucose on the function of Cav3.2, known to regulate secretory function, in neuroendocrine-like differentiated prostate cancer LNCaP cells. High glucose accelerated the increased channel function and overexpression of Cav3.2 during neuroendocrine differentiation, the former prevented by enzymatic inhibition of N-glycosylation and cleavage of N-glycans. Hyperglycemia thus appears to induce N-linked glycosylation-mediated functional upregulation and overexpression of Cav3.2 in neuroendocrine-like differentiated prostate cancer cells.

Keywords: Asparagine-linked glycosylation; Ca(v)3.2 T-type calcium channel; Prostate cancer.

MeSH terms

  • 1-Methyl-3-isobutylxanthine / pharmacology
  • Bucladesine / pharmacology
  • Calcium Channels, T-Type / biosynthesis*
  • Cell Differentiation*
  • Cell Line, Tumor
  • Gene Expression Regulation, Neoplastic*
  • Glucose / pharmacology*
  • Glycosylation / drug effects
  • Humans
  • Male
  • Membrane Potentials / drug effects
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / pathology*
  • Tunicamycin / pharmacology
  • Up-Regulation / drug effects*

Substances

  • CACNA1H protein, human
  • Calcium Channels, T-Type
  • Tunicamycin
  • Bucladesine
  • Glucose
  • 1-Methyl-3-isobutylxanthine