[Effect of NGX6 on gene expression profile of colon carcinoma cell line HT-29]

Ai Zheng. 2005 Sep;24(9):1064-70.
[Article in Chinese]

Abstract

Background & objective: Colon cancer is one of the most common malignant tumors, but the mechanism involved in its pathogenesis is not fully understood. Under the foundation of early study, we intended to explore the effects of NGX6 on the gene expression profile of colon carcinoma cell line HT-29.

Methods: pcDNA3.1-NGX6-transfected HT-29 cells were used as the test, and empty vector-transfected HT-29 cells were used as the control. Differentially expressed genes were screened with high-throughout BiostarH-80sx1 DNA microarray; part of the results of DNA microarray was confirmed by reverse transcription-polymerase chain reaction (RT-PCR).

Results: NGX6 transfection induced wide changes of the gene expression profile of HT-29 cells. A total of 377 genes were up-regulated or down-regulated by more than 3 folds, which were involved in cell signal transduction, cell cycle controlling, cell apoptosis, cytokinetics, gene transcription and translation, DNA damage and repairing, protein synthesis, metabolism, and so on. Some of them belonged to some important signal pathways related with cell proliferation and metastasis, such as DDK1, ILK, MMP-1 and COL11A1 in Wnt/beta-catenin signal pathway, ILK in ILK signal pathway, EpHB2 in Eph-Ephrins signal pathway, ROCK2 in RhoA signal pathway, RANBP1 in RanGTPase signal pathway, and RBBP1 in RB/RBBP1 signal pathway.

Conclusion: NGX6 transfection leads to molecular changes of some important signal pathways, and may suppress cell proliferation and metastasis of tumor by regulating these signal pathways.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Proliferation*
  • Gene Expression Profiling*
  • Gene Expression Regulation, Neoplastic
  • HT29 Cells
  • Humans
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Neoplasm Metastasis / genetics*
  • Signal Transduction*
  • Transfection
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism*

Substances

  • Membrane Proteins
  • TMEM8B protein, human
  • Tumor Suppressor Proteins