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Overexpression of Dickkopf-3 induces apoptosis through mitochondrial pathway in human colon cancer

Zi-Rong Yang1, Wei-Guo Dong, Xiao-Fei Lei

  • 1Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.

World Journal of Gastroenterology
|April 25, 2012
PubMed
Abstract

Insights

Dickkopf-3 (Dkk-3) overexpression inhibits colon cancer cell proliferation and invasion. This suggests Dkk-3 plays a role in apoptosis and the Wnt/β-catenin pathway, offering potential therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Colon cancer is a leading cause of cancer-related mortality worldwide.
  • Dickkopf-3 (Dkk-3) is a secreted protein implicated in various biological processes.
  • The specific roles of Dkk-3 in colon cancer progression, particularly in cell invasion and survival, require further elucidation.

Purpose of the Study:

  • To investigate the biological functions of Dickkopf-3 (Dkk-3) in colon cancer.
  • To elucidate the mechanisms underlying Dkk-3's effects on cell invasion, survival, and apoptosis in colon cancer cells.
  • To explore the potential involvement of Dkk-3 in the Wnt/β-catenin signaling pathway.

Main Methods:

  • Utilized three human colon cancer cell lines (HT-29, LoVo, SW480).
  • Overexpressed Dkk-3 in LoVo cells using pEGFP-N1-Dkk-3-GFP plasmid and Lipofectamine 2000.
  • Assessed Dkk-3 mRNA and protein levels via RT-PCR and Western blotting.
  • Evaluated cell proliferation, cell cycle, apoptosis (Hoechst 33258 assay), and invasion (Matrigel assay) in Dkk-3 overexpressing cells.

Main Results:

  • Dkk-3 expression was significantly lower in HT-29 and LoVo cells compared to SW480 cells, with LoVo cells exhibiting higher invasiveness.
  • Dkk-3 overexpression in LoVo cells suppressed proliferation and invasion, induced G(0)/G(1) cell cycle arrest, and promoted apoptosis.
  • Apoptosis was evidenced by increased chromatin condensation, elevated Bax and cytochrome c, decreased survivin and Bcl-2, and activated caspase-3/9. Cytosolic β-catenin levels were reduced.

Conclusions:

  • Dkk-3 overexpression induces apoptosis in human colon cancer cells, potentially via the mitochondrial pathway.
  • Dkk-3 appears to modulate colon cancer progression through its involvement in the Wnt/β-catenin signaling pathway.
  • Dkk-3 represents a potential therapeutic target for colon cancer treatment.
Keywords:
ApotosisColon cancerDickkopf-3InvasionMitochondriaOverexpression

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