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Chinese Journal of Breast Disease(Electronic Edition) ›› 2014, Vol. 08 ›› Issue (05): 16-18. doi: 10.3877/cma. j. issn.1674-0807.2014.05.004

• Original Articles • Previous Articles     Next Articles

Regulatory mechanism of oncogene RhoA on the expression of vascular epithelial growth factor in breast cancer cells

Qingli Zhao1,(), Ji Ma1   

  1. 1.Department of Breast Diseases, Lanzhou General Hospital of PLA, Lanzhou 730000, China
  • Received:2014-01-22 Online:2014-10-01 Published:2024-12-07
  • Contact: Qingli Zhao

Abstract:

Objective

To explore the effects of oncogene RhoA on protein expression of vascular epithelial growth factor(VEGF) and exocytosis in breast cancer cell line MDA-MB-231 and its potential molecular mechanism.

Methods

RhoA-overexpressed plasmid pcDNA3.0-V14RhoA, control plasmid pcDNA3.0 and RhoA-silencing plasmid pcDNA3.0-shRhoA were transfected into MDA-MB-231 cells. After that, VEGF protein expression was detected by Western blot and ELISA assay. The effects of RhoA on p53 expression and on VEGF regulation were examined by Western blot or real-time PCR. The means were compared using t text, and the measurement data were expressed as and processed using analysis of variance.

Results

After up-regulating RhoA in MDA-MB-231 cells, intracellular VEGF protein level and extracellular secretion level were significantly increased compared with the control group(F = 4.020,P =0.032), while after down-regulating RhoA in MDA-MB-231 cells, intracellular VEGF protein level and extracellular secretion level were significantly decreased compared with the control group(F = 5.131,P =0.001). Compared with the control group, the upregulation of RhoA could inhibit p53 expression (48 h:F=3.231,P=0.043)and the decrease of p53 expression could promote VEGF expression(48 h:F=3.226,P=0.015).

Conclusion

In breast cancer MDA-MB-231 cells, the change of RhoA expression can cause the change of intracellular and extracellular VEGF expression, and RhoA may promote VEGF expression through inhibiting p53 expression.

Key words: Breast neoplasms, Vascular endothelial growth factors, RhoA; p53

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