期刊
ONCOGENE
卷 38, 期 27, 页码 5500-5515出版社
SPRINGERNATURE
DOI: 10.1038/s41388-019-0806-6
关键词
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资金
- National Natural Science Foundation of China [81370600]
- Program for Professor of Special Appointment (Eastern Scholar) at Shanghai Institutions of Higher Learning [TP2015022]
- Shanghai Pujiang Program [15PJ1404800]
- Innovation Program of Shanghai Municipal Education Commission [15ZZ056]
- Innovation Program for Ph.D. students in Shanghai Jiaotong University School of Medicine [BXJ201731]
Non-muscle myosin IIA (NMIIA) protein plays an important role in cell cytokinesis and cell migration. The role and underlying regulatory mechanisms of NMIIA in pancreatic cancer (PC) remain elusive. We found that NMIIA is highly expressed in PC tissues and contributes to PC poor progression by using open microarray datasets from the Gene Expression Omnibus (GEO), The Cancer Genome Atlas (TCGA), and PC tissue arrays. NMIIA regulates beta-catenin mediated EMT to promote the proliferation, migration, invasion, and sphere formation of PC cells in vitro and in vivo. NMIIA controls the beta-catenin transcriptional activity by interacting with beta-catenin. Moreover, MEK/ERK signaling is critical in MLC2 (Ser19) phosphorylation, which can mediate NMIIA activity and regulate Wnt/beta-catenin signaling. These findings highlight the significance of NMIIA in tumor regression and implicate NMIIA as a promising candidate for PC treatment.
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