Depletion of Cks1 and Cks2 expression compromises cell proliferation and enhance chemotherapy-induced apoptosis in HepG2 cells

Lingqing Lin, Zanxi Fang, Huayue Lin, Hanyu You, Jiajia Wang, Yuanhui Su, Fen Wang, Zhong Ying Zhang

Research output: Contribution to journalArticle

12 Scopus citations

Abstract

The present study explored the oncogenic roles of overexpressed Cks1 and Cks2 in human hepatocellular carcinoma cells. Gene expression of Cks1 and Cks2 in HepG2 cells was disrupted by siRNA or increased by cDNA transfection. Cell proliferation was assayed by CCK-8 analysis and cell counting. Cisplatin-induced apoptosis after transfection was measured by flow cytometry using Annexin V/propidium iodide (PI) double staining. Cell cycle changes after transfection were determined by flow cytometry with PI staining. Protein levels of Akt and GSK-3β were measured after transfection. The results revealed that HepG2 proliferation was decreased by depletion of endogenous Cks1 or Cks2, and increased by overexpression of Cks1 or Cks2. HepG2 apoptosis increased concordantly with the decline of Cks1 or Cks2 expression. Overexpression of Cks1 or Cks2 prevented cell apoptosis. Protein levels of p-Akt and p-GSK-3β were downregulated after RNA interference of Cks1 or Cks2. In conclusion, Cks1 and Cks2 promoted proliferation and prevented apoptosis of HepG2 cells. The Akt/GSK-3β-related PI3K/Akt signaling pathway may be a key signaling pathway that is involved in the regulation of cell growth and cell death.

Original languageEnglish (US)
Pages (from-to)26-32
Number of pages7
JournalOncology Reports
Volume35
Issue number1
DOIs
StatePublished - Jan 2016
Externally publishedYes

Keywords

  • Apoptosis
  • Cyclin-dependent kinase subunit
  • Hepatocellular carcinoma
  • Proliferation

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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