NMIIA promotes tumor growth and metastasis by activating the Wnt/[beta]-catenin signaling pathway and EMT in pancreatic cancer

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...

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Veröffentlicht in:Oncogene 2019-07, Vol.38 (27)
Hauptverfasser: Zhou, Pingting, Li, Yanyan, Li, Bo, Zhang, Meichao, Liu, Yuanhua, Yao, Yuan, Li, Dong
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Sprache:eng
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Zusammenfassung: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.
ISSN:0950-9232
DOI:10.1038/s41388-019-0806-6