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Sp1 is a transcription repressor to stanniocalcin-1 expression in TSA-treated human colon cancer cells, HT29

Alice Y S Law1, B H Y Yeung, L Y Ching

  • 1Department of Biology, Hong Kong Baptist University, Kowloon Tong, Hong Kong.

Journal of Cellular Biochemistry
|April 6, 2011
PubMed

Insights

Specificity protein 1 (Sp1) and retinoblastoma (Rb) repress stanniocalcin-1 (STC1) gene transcription in colon cancer cells. Inhibiting Sp1 or promoting Sp1 hyperphosphorylation synergistically increases STC1 levels and apoptosis.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Gene Regulation

Background:

  • Stanniocalcin-1 (STC1) is implicated in apoptosis in HT29 colon cancer cells following histone deacetylase (HDAC) inhibitor treatment.
  • The precise mechanisms regulating STC1 expression in response to HDAC inhibitors require further elucidation.

Purpose of the Study:

  • To investigate the role of specificity protein 1 (Sp1) and retinoblastoma (Rb) in regulating STC1 gene transcription in trichostatin A (TSA)-treated HT29 cells.
  • To explore the therapeutic potential of targeting Sp1 in combination with HDAC inhibitors for colon cancer treatment.

Main Methods:

  • Cell culture of HT29 human colon cancer cells.
  • Treatment with TSA, Sp1 inhibitor mithramycin A (MTM), and protein phosphatase inhibitor okadaic acid (OKA).
  • Gene expression analysis (STC1 transcript levels, luciferase activity), apoptosis assays, Sp1 knockdown, chromatin immunoprecipitation (ChIP), and re-ChIP assays.

Main Results:

  • Sp1, in association with Rb, represses STC1 gene transcription in TSA-treated HT29 cells.
  • Co-treatment with TSA and MTM synergistically enhances STC1 expression and apoptosis.
  • Sp1 hyperphosphorylation, induced by OKA, reduces its transcriptional activity, leading to increased STC1 expression.
  • ChIP and re-ChIP assays confirm Sp1 binding to the STC1 promoter and recruitment of Rb.

Conclusions:

  • STC1 is identified as a downstream target gene regulated by Sp1.
  • Sp1 acts as a transcriptional repressor of STC1, with its activity modulated by phosphorylation and Rb association.
  • Targeting the Sp1/Rb/STC1 pathway presents a potential therapeutic strategy for colon cancer.

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