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MicroRNA-361 reduces the viability and migratory ability of pancreatic cancer cells via mediation of the MAPK/JNK pathway
Previous research has revealed that microRNA-361 (miR-361) functions as a fundamental modulator in non-small-cell lung cancer and esophageal carcinoma. However, its involvement in pancreatic cancer (PC) is yet to be elucidated. Therefore, the present study aimed to examine the mechanism and function...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8515516/ https://www.ncbi.nlm.nih.gov/pubmed/34659511 http://dx.doi.org/10.3892/etm.2021.10799 |
Sumario: | Previous research has revealed that microRNA-361 (miR-361) functions as a fundamental modulator in non-small-cell lung cancer and esophageal carcinoma. However, its involvement in pancreatic cancer (PC) is yet to be elucidated. Therefore, the present study aimed to examine the mechanism and function of miR-361 during the regulation of PC cell migration and viability. It was demonstrated that miR-361 expression decreased in PC cell lines and tissues, and the overexpression of miR-361 suppressed in vivo PC cell proliferation in mice. Moreover, flow cytometry and MTT assays indicated that the miR-361 mimic decreased the viability and increased the apoptosis of PC cells. Both Transwell migration and wound healing assays identified that miR-361 ameliorated the migratory ability of PC cells. Using dual-luciferase reporter assays, it was found that miR-361 targeted mitogen-activated protein kinase (MAPK)/JNK 3'-untranslated regions, inducing the downregulation of this gene. In PC cells, overexpression of MAPK/JNK diminished the pro-apoptotic effect of the miR-361 mimic, while restoring the migratory activity of PC cells. Collectively, the present results suggested novel molecular mechanisms underlying PC progression and development. |
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