[Construction of a eukaryotic vector expressing E2F-1 Gene and its effect on proliferation of gastric cancer cell line MKN-45]

Ai Zheng. 2007 Oct;26(10):1064-8.
[Article in Chinese]

Abstract

Background & objective: E2F-1 is overexpressed in many tumors and functions as an oncogene or tumor suppressor gene. This study was to construct the recombinant eukaryotic vector expressing E2F-1 cDNA, and explore the effect of E2F-1 overexpression on the proliferation of human gastric carcinoma cell line MKN-45.

Methods: The fragment of E2F-1 gene was amplified by polymerase chain reaction (PCR). A eukaryotic vector expressing E2F-1 (pCMV-E2F1-HA) was constructed with pCMV-HA, and transfected into COS-7 cells to identify whether E2F-1 was successfully subcloned into the eukaryotic vector. pCMV-E2F1-HA was transfected into MKN-45 cells. The expression of E2F-1 in MKN-45 cells was detected by Western blot. The proliferation of MKN-45 cells was observed by colony formation assay and MTS method. Cell cycle was analyzed by flow cytometry (FCM).

Results: Recombinant plasmid pCMV-E2F1-HA was successfully constructed and transfected into COS-7 and MKN-45 cells. MKN-45 cell clones were significantly fewer in pCMV-E2F1-HA group than in pCMV-HA group (4.7+/-1.8 vs. 30.2+/-6.7, P<0.01). The proliferation rate of MKN-45 cells was significantly lower in pCMV-E2F1-HA group (73.5% on Day 5, 63.5% on Day 6, 56.1% on Day 7) than in pCMV-HA group (100%, P<0.01). The G0/G1 phase proportion of MKN-45 cells was significantly higher in pCMV-E2F1-HA group than in pCMV-HA group (71.4% vs. 59.7%, P<0.05); the S phase proportion was significantly lower in pCMV-E2F1-HA group than in pCMV-HA group (18.7% vs. 30.7%, P<0.05).

Conclusion: Overexpression of E2F-1 suppresses the proliferation of gastric cancer MKN-45 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • COS Cells
  • Cell Cycle*
  • Cell Line, Tumor
  • Cell Proliferation*
  • Chlorocebus aethiops
  • E2F1 Transcription Factor / genetics
  • E2F1 Transcription Factor / metabolism*
  • Gene Expression Regulation, Neoplastic
  • Genetic Vectors
  • Humans
  • Plasmids
  • Stomach Neoplasms / metabolism
  • Stomach Neoplasms / pathology*
  • Transfection
  • Up-Regulation

Substances

  • E2F1 Transcription Factor
  • E2F1 protein, human