Silencing of TRPC1 regulates store-operated calcium entry and proliferation in Huh7 hepatocellular carcinoma cells

Selli C., ERAÇ Y., KOSOVA B., Erdal E. S., Tosun M.

BIOMEDICINE & PHARMACOTHERAPY, vol.71, pp.194-200, 2015 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 71
  • Publication Date: 2015
  • Doi Number: 10.1016/j.biopha.2015.02.024
  • Journal Name: BIOMEDICINE & PHARMACOTHERAPY
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.194-200
  • Keywords: Calcium store depletion, Cell proliferation, Fura-2, TRP channels, SMOOTH-MUSCLE-CELLS, RECEPTOR POTENTIAL CHANNELS, CAPACITATIVE CA2+ ENTRY, ENDOTHELIAL-CELLS, GROWTH, EXPRESSION, MECHANISMS, APOPTOSIS, CURRENTS, DISEASE
  • Dokuz Eylül University Affiliated: Yes

Abstract

Purpose: Previously, we observed reciprocal changes in TRPC1 and TRPC6 expression levels in aging rat aorta and A7r5, rat embryonic vascular smooth muscle cells. Furthermore, downregulation of TRPC1 significantly elevated store-operated Ca2+ entry suggesting the regulatory role of TRPC1 in A7r5 cells. Since TRPC6 upregulation shown to be associated with cell proliferation, the purpose of our study was to investigate the functional consequences of TRPC1 ion channel downregulation by RNA interference in Huh7 human hepatocellular carcinoma cell line.