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miRNA-7515 suppresses pancreatic cancer cell proliferation, migration and invasion via downregulating IGF-1 expression
Pancreatic cancer (PC) is a lethal malignancy of the gastrointestinal tract. Previous studies have reported that microRNAs (miRNAs/miRs) are involved in the tumorigenesis of PC. Therefore, the present study aimed to determine the effects of miR-7515 on PC cell proliferation, invasion and migration i...
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/PMC8317166/ https://www.ncbi.nlm.nih.gov/pubmed/34296285 http://dx.doi.org/10.3892/or.2021.8151 |
Sumario: | Pancreatic cancer (PC) is a lethal malignancy of the gastrointestinal tract. Previous studies have reported that microRNAs (miRNAs/miRs) are involved in the tumorigenesis of PC. Therefore, the present study aimed to determine the effects of miR-7515 on PC cell proliferation, invasion and migration in vitro and in vivo, and investigate its underlying molecular mechanism using bioinformatics, double luciferase assay and western blotting. The results revealed that the expression levels of miR-7515 were downregulated in PC, which predicted a poor clinical outcome. The overexpression of miR-7515 significantly decreased the proliferation, invasive and migratory abilities of PC cells in vitro and in vivo, while the knockdown of miR-7515 exerted the opposite effects. miR-7515 was identified to directly bind to insulin-like growth factor 1 (IGF-1) and downregulate its expression, which subsequently downregulated the Ras/Raf/MEK/ERK signalling pathway. The overexpression of IGF-1 reversed the inhibitory effects of miR-7515 overexpression on PC cells. In conclusion, the findings of the present study indicated that miR-7515 may act as a tumor suppressor in PC, as it repressed PC cell proliferation invasion and migration via downregulating the expression of IGF-1 and the activity of the Ras/Raf/MEK/ERK signalling pathways. |
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