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Snail interacts with hPLSCR1 promoter and down regulates its expression in IMR-32

Vincent Gerard Francis1, Purnima Padmanabhan1, Sathyanarayana N Gummadi1

  • 1Applied and Industrial Microbiology Laboratory, Department of Biotechnology, Indian Institute of Technology Madras, Chennai 600 036, India.

Biochemical and Biophysical Research Communications
|June 1, 2014
PubMed

Insights

The Snail transcription factor (TF) binds to the human phospholipid scramblase 1 (hPLSCR1) promoter, downregulating its expression. This discovery reveals a novel mechanism influencing hPLSCR1 levels and has implications for cancer progression.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Gene Regulation

Background:

  • Human phospholipid scramblase 1 (hPLSCR1) is a proapoptotic protein.
  • Deregulation of hPLSCR1 expression is observed in various cancer cells.
  • The transcriptional regulation of hPLSCR1 remains largely unknown.

Purpose of the Study:

  • To investigate the transcriptional regulation of hPLSCR1.
  • To identify specific regulatory regions and transcription factors involved in hPLSCR1 expression.
  • To elucidate the role of Snail transcription factor in hPLSCR1 regulation.

Main Methods:

  • Cloning and analysis of the 5'-flanking region of hPLSCR1.
  • Luciferase reporter assays to determine promoter activity.
  • Snail knockdown using Snail-shRNA, point mutation studies, and Chromatin Immunoprecipitation (ChIP) assays.

Main Results:

  • A key regulatory region (-1525 to -1244) of the hPLSCR1 promoter was identified.
  • A Snail transcription factor (TF) binding site within this region was found to downregulate hPLSCR1 expression.
  • Snail specifically binds to the -1123 to -1117 site on the hPLSCR1 promoter, confirmed by ChIP assay.

Conclusions:

  • This study identifies Snail TF as a novel transcriptional regulator of hPLSCR1.
  • Snail-mediated downregulation of hPLSCR1 has potential implications in cancer progression.
  • This finding provides new insights into the molecular mechanisms underlying hPLSCR1 dysregulation in cancer.
Keywords:
ChIPPromoterSnailTranscriptional regulationhPLSCR1

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