Proteomic analysis of differential proteins in pancreatic carcinomas: Effects of MBD1 knock-down by stable RNA interference

BMC Cancer. 2008 Apr 29:8:121. doi: 10.1186/1471-2407-8-121.

Abstract

Background: Methyl-CpG binding domain protein 1 (MBD1), a suppressor of gene transcription, may be involved in inactivation of tumor suppressor genes during tumorigenesis. Over-expression of MBD1 has been reported in human pancreatic carcinomas.

Methods: In this study, we established a MBD1-knock-down pancreatic cancer cell line (BxPC-3) using stable RNA interference, to compare the proteomic changes between control and MBD1-knock-down cells using two-dimensional gel electrophoresis and mass spectrometry.

Results: We identified five proteins that were up-regulated and nine proteins that were down-regulated. Most of the identified proteins are involved in tumorigenesis, some are prognostic biomarkers for human malignant tumors.

Conclusion: Our data suggest that these differential proteins may be associated with the function of MBD1, and provide some insight into the functional mechanism of MBD1 in the development of pancreatic cancer.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biomarkers, Tumor / genetics
  • Cell Line, Tumor
  • DNA-Binding Proteins / antagonists & inhibitors
  • DNA-Binding Proteins / biosynthesis
  • DNA-Binding Proteins / genetics*
  • Electrophoresis, Gel, Two-Dimensional
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Pancreatic Neoplasms / genetics*
  • Pancreatic Neoplasms / pathology
  • Proteomics
  • RNA Interference
  • RNA, Small Interfering / administration & dosage
  • RNA, Small Interfering / genetics*
  • Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
  • Transcription Factors / antagonists & inhibitors
  • Transcription Factors / biosynthesis
  • Transcription Factors / genetics*

Substances

  • Biomarkers, Tumor
  • DNA-Binding Proteins
  • MBD1 protein, human
  • RNA, Small Interfering
  • Transcription Factors