PNAS-4 expression and its relationship to p53 in colorectal cancer

Mol Biol Rep. 2012 Jan;39(1):243-9. doi: 10.1007/s11033-011-0732-3. Epub 2011 May 10.

Abstract

PNAS-4 is a novel pro-apoptotic protein activated during the early response to DNA damage; however, the molecular mechanisms and pathways regulating PNAS-4 expression in tumors are not well understood. We hypothesized that PNAS-4 is a p53 down-stream target gene and designed this study. We searched online for putative p53-binding sites in the entire PNAS-4 gene and did not find any corresponding information. In HCT116 colon cancer cells, after being transfected with small interfering RNA to silence p53, the expressions of PNAS-4 and other known p53 target gene (Apaf1, Bax, Fas and Dr5) were determined by real-time PCR. We found that PNAS-4 was up-regulated while Apaf1, Bax, Fas and Dr5 were down-regulated. We then examined the expression of PNAS-4 and p53 mutation in colorectal cancer patients. PNAS-4 expressed both in colorectal cancers and normal tissues, but compared with paired control, PNAS-4 was up-regulated in cancers (P=0.018). PNAS-4 overexpression ratios were correlated to the p53 mutant status (P=0.001). The mean PNAS-4 expression levels of p53 mutant homozygote group and heterozygote group were higher than that of p53 wild type group (P=0.013). The expression ratios of PNAS-4 (every sample in relative to its paired normal mucosa) were different between negative lymph node metastasis (66% up-regulated, 34% down-regulated) and positive metastasis (42% up-regulated, 58% down-regulated). Taken together, these findings suggested that PNAS-4 was not a p53 target, but overexpression of PNAS-4 was correlated to p53 inactivity in colorectal cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Apoptosis Regulatory Proteins / genetics
  • Apoptosis Regulatory Proteins / metabolism*
  • Carbon-Nitrogen Lyases
  • Cell Line, Tumor
  • Colorectal Neoplasms / genetics*
  • DNA Primers / genetics
  • DNA, Complementary / genetics
  • Gene Expression Regulation, Neoplastic / genetics*
  • Humans
  • Middle Aged
  • Mutation / genetics
  • Protein Interaction Domains and Motifs / genetics*
  • RNA, Small Interfering / genetics
  • Real-Time Polymerase Chain Reaction
  • Statistics, Nonparametric
  • Transfection
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Apoptosis Regulatory Proteins
  • DNA Primers
  • DNA, Complementary
  • RNA, Small Interfering
  • Tumor Suppressor Protein p53
  • Carbon-Nitrogen Lyases
  • DESI2 protein, human