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Effect of indomethacin on E-cadherin and beta-catenin expression in HT-29 colon cancer cells

Sanja Kapitanović1, Tamara Cacev, Mariastefania Antica

  • 1Division of Molecular Medicine, Ruder Bosković Institute, Bijenicka c. 54, HR-10000 Zagreb, Croatia. kapitan@irb.hr

Experimental and Molecular Pathology
|June 21, 2005
PubMed

Insights

Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit colon cancer growth by inducing apoptosis and altering Wnt signaling pathways. Indomethacin enhances cell adhesion through increased E-cadherin and beta-catenin translocation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs) are known to reduce colon cancer incidence and mortality.
  • The precise molecular mechanisms underlying the antitumor effects of NSAIDs, particularly their impact on Wnt signaling, remain largely unelucidated.

Purpose of the Study:

  • To investigate the effects of indomethacin, an NSAID, on colon cancer cell proliferation, apoptosis, and Wnt signaling gene expression.
  • To elucidate the role of indomethacin in modulating key proteins and genes within the Wnt pathway in HT-29 colon cancer cells.

Main Methods:

  • HT-29 colon cancer cells were treated with varying concentrations of indomethacin.
  • Cell proliferation and apoptosis were assessed.
  • Expression levels of APC, beta-catenin, and E-cadherin proteins were analyzed.
  • Gene expression levels of APC and E-cadherin were confirmed using real-time RT-PCR.

Main Results:

  • Indomethacin significantly inhibited HT-29 cell proliferation and induced apoptosis in a dose- and time-dependent manner.
  • Treatment with indomethacin led to enhanced expression of APC and E-cadherin, while beta-catenin was translocated from the nucleus/cytoplasm to the plasma membrane.
  • Real-time RT-PCR confirmed increased mRNA levels for APC (10.9-fold) and E-cadherin (3.5-fold) at 4 x 10(-4) M indomethacin.

Conclusions:

  • Indomethacin exhibits antiproliferative effects on colon cancer cells, partly mediated by inducing apoptosis.
  • The observed effects suggest that indomethacin enhances cell adhesion by upregulating E-cadherin and promoting beta-catenin translocation to the cell membrane.
  • These findings provide insights into the molecular mechanisms by which NSAIDs may exert their chemopreventive and therapeutic effects in colon cancer.

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