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Acta Pharmacol Sin. 2010 Jun;31(6):725-32. doi: 10.1038/aps.2010.56. Epub 2010 May 10.

Myosin light chain kinase is responsible for high proliferative ability of breast cancer cells via anti-apoptosis involving p38 pathway.

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  • 1Department of Biochemistry, the Key Laboratory of Bioactive Materials, Ministry of Education, College of Life Sciences, Nankai University, Tianjin, China.



To investigate whether myosin light chain kinase (MLCK) contributed to the high proliferative ability of breast cancer cells.


Soft agar colony formation on the MCF-7 and LM-MCF-7 cell lines was determined. The cell cycles of MCF-7 and LM-MCF-7 were detected using flow cytometry analysis. Western blot analysis was performed to detect the expression levels of p-ERK1/2, total-ERK1/2, p-p38, total p38, p-JNK, total-JNK, survivin, Bcl-2, p-MLC, caspase-9, cleaved caspase-9, and MLCK. After treatment with adriamycin (ADR), ML-7 and SB203580, apoptosis was examined using flow cytometry analysis and Annexin V-FITC fluorescence microscopy.


The breast cancer LM-MCF-7 cell line with high metastasis potential (a metastitic sub-clone of MCF-7) had higher anti-apoptosis ability relative to MCF-7 cells in response to adriamycin treatment (apoptosis rate: 6.76% vs 28.58%, P<0.05). Moreover, the expression level of MLCK was upregulated and the level of phosphorylated p38 (p-p38) was decreased in LM-MCF-7 cells. Flow cytometry analysis showed that ML-7, selective inhibitor of MLCK, could induce apoptosis of the LM-MCF-7 cells, in which the level of p-p38 was increased. Meanwhile, the expression levels of Bcl-2 and survivin were downregulated, while the caspase-9 was upregulated suggesting that the cells were undergone apoptosis. Flow cytometry analysis showed that SB203580, an inhibitor of p38, abolished ML-7-induced apoptosis, which resulted in the upregulation of Bcl-2 and survivin, and downregulation of caspase-9, suggesting that Bcl-2, survivin and caspase-9 are downstream effectors of p38.


MLCK is responsible for high proliferative ability of breast cancer cells through anti-apoptosis, in which p38 pathway was involved.

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