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Targeting HOX and PBX transcription factors in ovarian cancer

Richard Morgan1, Lynn Plowright, Kevin J Harrington

  • 1Postgraduate Medical School, University of Surrey, Guildford, UK. r.morgan@surrey.ac.uk

BMC Cancer
|March 12, 2010
PubMed
Abstract

Insights

Dysregulated HOX gene expression drives ovarian cancer progression. Disrupting HOX/PBX interactions halts tumor growth and induces cell death, identifying a novel therapeutic target for ovarian cancer.

Area of Science:

  • Molecular Biology
  • Genetics
  • Oncology

Background:

  • Ovarian cancer has a poor prognosis due to drug resistance, necessitating new therapeutic targets.
  • HOX genes, crucial for embryonic development, also play roles in cancer cell survival and proliferation.
  • These genes have demonstrated anti-apoptotic functions in various cancers, including lung and renal.

Purpose of the Study:

  • To investigate the role of HOX genes in ovarian cancer cell survival and proliferation.
  • To identify potential therapeutic targets for ovarian cancer treatment.

Main Methods:

  • Quantitative PCR (QPCR) was used to assess HOX gene expression in normal ovarian tissue and ovarian cancer cell lines (SK-OV3, OV-90).
  • A peptide, HXR9, was employed to disrupt HOX/PBX dimer formation and alter HOX protein transcriptional regulation.

Main Results:

  • The SK-OV3 ovarian cancer cell line displayed significantly dysregulated HOX gene expression, unlike the OV-90 line.
  • Inhibition of HOX/PBX interactions led to apoptosis in SK-OV3 cells.
  • Disrupting HOX/PBX binding also retarded tumor growth in vivo.

Conclusions:

  • HOX/PBX binding represents a promising therapeutic target for ovarian cancer.
  • Targeting HOX/PBX interactions offers a potential strategy to overcome drug resistance and improve patient outcomes.

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