关键词: 三阴性乳腺癌, 蛋白激酶, 迁移, 侵袭

Abstract:

Background and purpose: Triple-negative breast cancer (TNBC) possesses high risk of relapse and metastasis. Clinically, there are no specific targeted-therapies to TNBC except chemotherapy. Therefore, studying the mechanism of relapse and metastasis has significance to improve the patients’ survival rate. This experiment aimed to study the effect of MAPK activation on migration and invasion of triple-negative breast cancer cells. Methods: Difference of migration and invasion between lung-high metastasis breast cancer cell line 231-HM and its parental cell line 231-p were first examined by cell scratch and transwell; Then, metastasis-associated proteins and MAPKassociated molecules were detected by Western blot; Last, 231-p cells were treated with P38/MAPK inhibitor and used to determine cell migration, invasion, and metastasis-associated proteins thereafter. Results: Compared with the parental cell line 231-p, 231-HM cells displayed obviously higher ability of migration and invasion. With the increased expression of Caveolin-1and β-catenin, the phosphorylation of MAPK-associated molecules including P38, Erk1/2, and MEK was highly decreased. Treatment of 231-p cells with low concentration (10 μmol/L) of the P38/MAPK inhibitor SB202190 increased the migration and invasion of 231-p cells, and the expression of Caveolin-1 and β-catenin. Conclusion: Activation of MAPK signaling inhibits the migration and invasion of triple-negative breast cancer.

Key words: Triple-negative breast cancer, MAPK, Migration, Invasion