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Trichostatin A-induced apoptosis is mediated by Kruppel-like factor 4 in ovarian and lung cancer

Sadeghi Zohre1, Nejati-Koshki Kazem, Akbarzadeh Abolfazl

  • 1Hematology and Oncology Research Center, Tabriz, Iran

Asian Pacific Journal of Cancer Prevention : APJCP
|August 30, 2014
PubMed
Abstract

Insights

Trichostatin A (TSA) increases Kruppel-like factor 4 (klf4) expression, inhibiting cancer cell growth and promoting apoptosis in ovarian and lung cancer cells. This suggests klf4 acts as a tumor suppressor in response to HDAC inhibition.

Area of Science:

  • Cancer Biology
  • Molecular Oncology
  • Epigenetics

Background:

  • Histone deacetylase (HDAC) inhibitors like trichostatin A (TSA) regulate gene expression and inhibit cancer cell proliferation.
  • Kruppel-like factor 4 (klf4) is a transcription factor involved in cell proliferation, differentiation, tumorigenesis, and apoptosis, with context-dependent roles in cancer.

Purpose of the Study:

  • To investigate if TSA upregulates klf4 expression and induces growth inhibition and apoptosis in SKOV-3 (ovarian) and A549 (lung) cancer cell lines.
  • To explore the molecular mechanisms underlying HDAC inhibitor-induced effects on cancer cells.

Main Methods:

  • Cytotoxicity assessed using MTT assay.
  • klf4 gene expression analyzed by real-time PCR.
  • Apoptosis induction evaluated via Vybrant Apoptosis Assay kit and flow cytometry.

Main Results:

  • TSA demonstrated dose- and time-dependent cytotoxicity against SKOV-3 and A549 cells.
  • TSA treatment led to increased klf4 expression.
  • Flow cytometry confirmed elevated apoptosis levels post-TSA treatment.

Conclusions:

  • TSA upregulates klf4 expression in SKOV-3 and A549 cells, suggesting klf4 plays a tumor-suppressive role.
  • Increased klf4 expression contributes to TSA-mediated cell growth inhibition and apoptosis.
  • This study elucidates molecular mechanisms of HDAC inhibitor action, including cell cycle arrest and apoptosis induction.

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