Mesothelin promotes invasion and metastasis in breast cancer cells
Y Wang, L Wang, D Li, HB Wang… - Journal of International …, 2012 - journals.sagepub.com
Y Wang, L Wang, D Li, HB Wang, QF Chen
Journal of International Medical Research, 2012•journals.sagepub.comObjective: The presence of mesothelin (encoded by the mesothelin [MSLN] gene) in breast
cancer is associated with tumour infiltration of the lymph node. This study evaluated whether
MSLN overexpression promotes breast cancer cell invasiveness and metastasis. Methods:
This study evaluated the effects of overexpression of MSLN on extracellular signal-regulated
kinase (ERK1/2) and matrix metalloproteinase (MMP)-9 levels, and the invasiveness and
angiogenesis of the breast cancer cell line MCF-7 in vitro, and on MCF-7-derived tumour …
cancer is associated with tumour infiltration of the lymph node. This study evaluated whether
MSLN overexpression promotes breast cancer cell invasiveness and metastasis. Methods:
This study evaluated the effects of overexpression of MSLN on extracellular signal-regulated
kinase (ERK1/2) and matrix metalloproteinase (MMP)-9 levels, and the invasiveness and
angiogenesis of the breast cancer cell line MCF-7 in vitro, and on MCF-7-derived tumour …
Objective
The presence of mesothelin (encoded by the mesothelin [MSLN] gene) in breast cancer is associated with tumour infiltration of the lymph node. This study evaluated whether MSLN overexpression promotes breast cancer cell invasiveness and metastasis.
Methods
This study evaluated the effects of overexpression of MSLN on extracellular signal-regulated kinase (ERK1/2) and matrix metalloproteinase (MMP)-9 levels, and the invasiveness and angiogenesis of the breast cancer cell line MCF-7 in vitro, and on MCF-7-derived tumour development in vivo.
Results
MSLN overexpression significantly increased ERK1/2 and MMP-9 protein levels and activity, and the invasive and angiogenic capability of MCF-7 cells, in vitro. Inhibition of ERK1/2 suppressed MMP-9 and the invasive and angiogenic capability of MSLN overexpressing MCF-7 cells. MSLN overexpression also increased MCF-7-derived tumour metastasis in vivo.
Conclusion
MSLN overexpression promoted the invasive potential of MCF-7 cells through ERK1/2-dependent upregulation of MMP-9; this association may have contributed to metastasis of MCF-7 cells in vivo. Mesothelin may be a useful biomarker for cancer progression and a novel therapeutic or chemopreventive target in human breast cancer.
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