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Updated: Feb 23, 2026

SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry
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LRF inhibits p53 expression in colon cancer cells via modulating DAP5 activity

Min Zhu1, Peng Wang1, Fan Feng2

  • 1Department of Oncology, Nan Lou Division, Chinese PLA General Hospital, Beijing, China.

Cell Biochemistry and Function
|August 30, 2017
PubMed

Insights

Leukaemia/lymphoma-related factor (LRF) promotes colon cancer growth by inhibiting p53 expression. Protease-activated receptor 2 (PAR2) activation increases LRF, which interacts with DAP5 to repress p53, suggesting LRF as a potential colon cancer treatment target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The p53 protein is crucial for tumor suppression, but its regulation is not fully understood.
  • Leukaemia/lymphoma-related factor (LRF) is known to promote tumor cell growth.

Purpose of the Study:

  • To investigate the hypothesis that LRF inhibits p53 expression in colon cancer cells.
  • To explore the role of protease-activated receptor 2 (PAR2) in regulating LRF and p53 expression.

Main Methods:

  • Utilized human colon cancer cell lines (LIM1215 and HCT116).
  • Analyzed gene expression using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting.
  • Investigated protein-protein interactions using co-immunoprecipitation or similar techniques.

Main Results:

  • Protease-activated receptor 2 (PAR2) expression was detected in colon cancer cells.
  • PAR2 activation led to increased LRF expression and decreased p53 expression.
  • A complex formed between LRF and DAP5, a p53 transcription factor, resulting in p53 repression.

Conclusions:

  • PAR2 activation upregulates LRF in colon cancer cells.
  • LRF interacts with DAP5 to inhibit p53 expression.
  • LRF represents a potential therapeutic target for colon cancer treatment.
Keywords:
DAP5LRFapoptosiscolon cancerp53 protein

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