Relationship Between HSP70 and ERBB2 Expression in Breast Cancer Cell Lines Regarding Drug Resistance

L U Yue1, Jin-Yu Xiang2, Ping Sun2

  • 1Department of Oncology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, Qingdao, P.R. China.

Anticancer Research
|March 16, 2016
PubMed
Abstract

Insights

Heat shock protein 70 (HSP70) affects human epidermal growth factor receptor-2 (ERBB2) expression and ERBB2-mediated drug resistance in breast cancer. Silencing HSP70 enhances sensitivity to fluorouracil treatment in SK-BR-3 cells.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Heat shock protein 70 (HSP70) is a downstream target of human epidermal growth factor receptor-2 (ERBB2).
  • The precise role of HSP70 in ERBB2-mediated drug resistance in breast cancer remains largely unexplored.

Purpose of the Study:

  • To investigate the relationship between HSP70 and ERBB2.
  • To determine the impact of HSP70 on ERBB2-mediated drug resistance in breast cancer cells.

Main Methods:

  • Breast cancer cells (SK-BR-3) were infected with lentivirus vectors to silence HSP70 (Lenti-ShHSP70) and ERBB2 (Lenti-ShERBB2).
  • Gene and protein expression levels of HSP70 and ERBB2 were analyzed using real-time polymerase chain reaction and western blotting.
  • Cell viability was assessed using the CCK8 assay to evaluate drug sensitivity.

Main Results:

  • Silencing HSP70 led to a significant down-regulation of both ERBB2 mRNA and protein levels in SK-BR-3 cells.
  • ERBB2 silencing also reduced HSP70 expression.
  • Inhibition of HSP70 increased the sensitivity of SK-BR-3 cells to fluorouracil treatment, as indicated by the CCK8 assay.

Conclusions:

  • HSP70 plays a crucial role in regulating ERBB2 expression.
  • HSP70 is implicated in ERBB2-mediated drug resistance in breast cancer.
  • Targeting HSP70 may represent a therapeutic strategy to overcome drug resistance in ERBB2-positive breast cancer.

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