Phosphorylation of myofibrillogenesis regulator‐1 activates the MAPK signaling pathway and induces proliferation and migration in human breast cancer MCF7 cells
Copyright policy )Phosphorylation of myofibrillogenesis regulator‐1 activates the MAPK signaling pathway and induces proliferation and migration in human breast cancer MCF7 cells
Myofibrillogenesis regulator‐1 (MR‐1) has been characterized as a tumor promoter in many cancers. However, its mechanism of action has not been fully elucidated. Here, we report that MR‐1 is overexpressed in human breast cancer cells and participates in tumor promotion in human breast cancer MCF7 cells by activating the ERK1/2 signaling pathway. MR‐1 interacts with MEK1/2 and ERK1, and its N‐terminal sequence plays a major role in promoting the MEK/ERK cascade. Furthermore, six phosphorylation sites of MR‐1 were identified, and phosphorylation at S46 was shown to be critical for the activation of MEK/ERK. Therefore, our findings suggest that MR‐1 functions as a tumor promoter in MCF7 cells by activating the MEK/ERK signaling.
- Chinese Academy of Medical Sciences & Peking Union Medical College China (People's Republic of)
- PEKING UNION MEDICAL COLLEGE China (People's Republic of)
MEK1/2, Base Sequence, Carcinogenesis, MAP Kinase Signaling System, Phosphorylation sites, Muscle Proteins, Breast Neoplasms, Myofibrillogenesis regulator 1, ERK1, Gene Expression Regulation, Neoplastic, Breast cancer, Cell Movement, MCF-7 Cells, Humans, Gene Silencing, Phosphorylation, RNA, Small Interfering, Cell Proliferation
MEK1/2, Base Sequence, Carcinogenesis, MAP Kinase Signaling System, Phosphorylation sites, Muscle Proteins, Breast Neoplasms, Myofibrillogenesis regulator 1, ERK1, Gene Expression Regulation, Neoplastic, Breast cancer, Cell Movement, MCF-7 Cells, Humans, Gene Silencing, Phosphorylation, RNA, Small Interfering, Cell Proliferation
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