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Conditional Knockdown of Gene Expression in Cancer Cell Lines to Study the Recruitment of Monocytes/Macrophages to the Tumor Microenvironment
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Down-regulation of survivin suppresses uro-plasminogen activator through transcription factor JunB

Kyung Hee Lee1, Eun Young Choi, Sung Ae Koh

  • 1Department of Hematology-Oncology, College of Medicine, Yeungnam University, Daegu 705-717, Korea.

Experimental & Molecular Medicine
|July 8, 2011
PubMed

Insights

Survivin, a key protein in cancer, promotes stomach cancer cell invasion and proliferation. Hepatocyte growth factor (HGF) upregulates survivin via JunB, making it a potential therapeutic target for gastric cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Survivin, an inhibitor of apoptosis protein, is implicated in cancer development but its clinical relevance is debated.
  • Hepatocyte growth factor (HGF) is known to influence cancer cell behavior.

Purpose of the Study:

  • To investigate the role of survivin in HGF-induced gene expression and its contribution to gastric cancer progression.
  • To elucidate the molecular mechanisms linking HGF, JunB, survivin, and uro-plasminogen activator (uPA) in gastric cancer cells.

Main Methods:

  • cDNA microarray analysis to screen HGF-induced genes in gastric cancer cell lines (NUGC3, MKN28).
  • Gene expression analysis (JunB, survivin, uPA) following HGF treatment and MEK inhibitor (PD 98059) pre-treatment.
  • Survivin and JunB knockdown experiments using shRNA.
  • Cell proliferation assays (MTT) and in vitro invasion assays (Matrigel).

Main Results:

  • HGF dose-dependently upregulated JunB, survivin, and uPA in gastric cancer cells.
  • MEK inhibitor PD 98059 blocked HGF-induced upregulation of JunB, survivin, and uPA.
  • Survivin knockdown reduced cell proliferation and invasion, and repressed HGF-induced uPA upregulation.
  • HGF enhanced JunB binding to the survivin promoter, an effect dependent on JunB expression.

Conclusions:

  • Survivin plays a critical role in HGF-mediated upregulation of uPA via JunB in gastric cancer.
  • Survivin contributes to HGF-induced tumor invasion and metastasis, suggesting it as a potential therapeutic target for gastric cancer.

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