Intracellular signaling pathways regulate hormone-dependent kallikrein gene expression

Tumour Biol. 2008;29(2):63-75. doi: 10.1159/000135686. Epub 2008 Jun 2.

Abstract

Objectives: Our aim was to examine how certain signal transduction pathways influence the regulation of hormone-dependent kallikrein (KLK) gene expression in androgen-sensitive breast cancer cell lines.

Methods: We used the breast cancer cell lines T47D and BT474, treated with steroid hormones or various pathway inhibitors. KLKs were quantified by ELISA. RT-PCR, Western blots and immunoprecipitations were used to assess transcript and protein levels.

Results: PSA, KLK10, KLK11, KLK13 and KLK14 are upregulated upon androgen stimulation in the T47D cell line. The expression of PSA, KLK10 and KLK11 was repressed by the MEK1/2 inhibitor U0126 and the PI3K inhibitor Wortmannin in the presence of the hormone, thus implicating the RAS/MEK/ERK and PI3K/AKT signaling pathways in regulating hormone-dependent KLK gene activation. Analysis of inhibitor-treated cells revealed changes in c-MYC expression with a pattern parallel to KLK gene expression. Chromatin immunoprecipitations identified androgen-dependent recruitment of specific transcription factors to the KLK proximal promoters, including c-MYC binding to PSA and KLK11.

Conclusion: The hormone-specific upregulation of PSA, KLK10 and KLK11 in the breast cancer cell line T47D is dependent on major intracellular signaling pathways. This work provides a new dimension to the regulation of these cancer-related genes and the potential for new therapeutic targeting strategies.

MeSH terms

  • Androgens / metabolism*
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Apoptosis / physiology
  • Breast Neoplasms / genetics
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Cell Line, Tumor
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Female
  • Gene Expression Regulation, Neoplastic / physiology*
  • Humans
  • Kallikreins / genetics
  • Kallikreins / metabolism*
  • MAP Kinase Kinase Kinases / metabolism
  • NF-kappa B / antagonists & inhibitors
  • Oncogene Protein v-akt / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Prostate-Specific Antigen / genetics
  • Prostate-Specific Antigen / metabolism
  • Proto-Oncogene Proteins c-myc / metabolism
  • Receptors, Androgen / metabolism
  • Serine Endopeptidases / genetics
  • Serine Endopeptidases / metabolism*
  • Sesquiterpenes / pharmacology
  • Signal Transduction / physiology*
  • Transcriptional Activation

Substances

  • Androgens
  • Anti-Inflammatory Agents, Non-Steroidal
  • MYC protein, human
  • NF-kappa B
  • Proto-Oncogene Proteins c-myc
  • Receptors, Androgen
  • Sesquiterpenes
  • trypsin-like serine protease
  • parthenolide
  • Phosphatidylinositol 3-Kinases
  • Oncogene Protein v-akt
  • Extracellular Signal-Regulated MAP Kinases
  • MAP Kinase Kinase Kinases
  • KLK10 protein, human
  • Kallikreins
  • Serine Endopeptidases
  • Prostate-Specific Antigen