CircPIP5K1A activates KRT80 and PI3K/AKT pathway to promote gastric cancer development through sponging miR-671-5p - 19/04/20
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Iconographies | 7 |
Vidéos | 0 |
Autres | 0 |
Highlights |
• | CircPIP5K1A promoted GC progression. |
• | CircPIP5K1A regulated GC development by sponging miR-671-5p. |
• | KRT80 was directly targeted by miR-671-5p in GC. |
• | CircPIP5K1A promoted GC progression by modulating KRT80. |
Abstract |
Background |
Gastric cancer (GC) has been regarded as a kind of the most common cancers in gastrointestinal malignant tumors. Circular RNA (circRNA) is a newly discovered category of non-coding RNAs and plays a significant role in the initiation or development of human cancers. Nevertheless, the role of circPIP5K1A in GC remains unclear.
Methods |
The relative expression level and the circular structure of circPIP5K1A were confirmedby RT-qPCR. The biological function of circPIP5K1A in GC was evaluated by colony formation, transwell and western blot assays. The binding capacity between miR-671-5p and circPIP5K1A (or KRT80) was assessed by luciferase reporter and Ago2-RIP assays. Protein levels of PI3K/AKT pathway were measured by western blot assay.
Results |
CircPIP5K1A was up-regulated in GC tissues and cells with a circular structure. Functionally, circPIP5K1A silence limited cell proliferation, invasion, migration and EMT process. Mechanistically, circPIP5K1A directly interacted with miR-671-5p to modulate KRT80 expression. Either miR-671-5p inhibitor or KRT80 overexpression could offset the inhibitory effect of circPIP5K1A depletion on GC development. Besides, circPIP5K1A played its oncogenic role in GC through regulating PI3K/AKT pathway. At last, circPIP5K1A promoted GC tumor growth in vivo.
Conclusions |
CircPIP5K1A/miR-671-5p/KRT80 axis contributes to GC progression through PI3K/AKT pathway, implying this axis may be a potential therapeutic target for the treatment of GC patients.
Le texte complet de cet article est disponible en PDF.Keywords : Gastric cancer, circPIP5K1A, miR-671-5p, KRT80, PI3K/AKT pathway
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