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Chinese Journal of Breast Disease(Electronic Edition) ›› 2009, Vol. 03 ›› Issue (01): 46-52. doi: 10.3877/cma.j.issn.1674-0807.2009.01.009

• Experimental Research • Previous Articles     Next Articles

Relationship between p38MAPK activity and apoptosis during drug resistance of breast carcinoma cell lines

Shao-bo ZENG1, Ming-yin LAN1, Zhi-yuan JIAN1, Heng LI1, Bin YAN1, Min ZHANG1, Meng ZHOU1, Bin JIANG,1()   

  1. 1.General Surgery of Taihe Hospital, Yunyang Medical College, Shiyan 442000, China
  • Received:2008-08-20 Online:2009-02-01 Published:2024-12-06
  • Contact: Bin JIANG

Abstract:

Objective

To investigate the relationship between p38MAPK activity and cell apoptosis and the effect of p38MAPK signal transduction pathway during drug resistance of breast carcinoma cell lines.

Methods

Flow cytometry (FCM) was used to analyze the effect of p38MAPK inhibitor SB203580 on the apoptosis of MCF-7/ADM cell, a drug resistant human breast cancer cell. The inhibition concentration 50% (IC50) of adriamycin on MCF-7/ADM was determined by MTT method in vitro.The MDR-1 mRNA level and p38MAPK protein expression in each group were detected by RT-PCR and Western Blot, respectively.

Results

After SB203580 action for 24 hours, the apoptosis rate of MCF-7/ADM was (26.73 ±4.90)%, which was significantly lower than that of the control group and the untreated group (F =143.80,P<0.001 ). The relative reverse rate of the sensitivity of MCF-7/ADM to adriamycin in the SB203580 treated group was 68.45%. The p38MAPK protein(F=685.42,P<0.001) and MDR-1 mRNA expression(F = 913 9. 24,P<0. 001) after 24-hour SB203580 action were markedly lower than the control group and the untreated group.

Conclusion

p38MAPK signal pathway plays an important role in drug resistance of breast carcinoma cell. p38MAPK can protect MCF-7/ADM cells from apoptosis, and blocking the p38MAPK signal pathway can increase the apoptosis in drug resistant breast carcinoma cell lines.

Key words: Breast carcinoma, Cell apoptosis, p38MAPK, Multidrug resistance

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