| Literature DB >> 31601147 |
Qing Liu1, Zhenting Wang1, Xiaohua Zhou2, Mingying Tang2, Wei Tan1, Tianshi Sun2, Youwen Deng1,2.
Abstract
Osteosarcoma (OS) accounts for 9 percent of cancer-related deaths in young people. The PI3K/Akt signaling, a well-known carcinogenic signaling pathway in human cancer, cooperates with other signaling pathways such as Wnt signaling to promote cancer progression. Wnt7b, as a transforming member of the Wnt family, could activate mTORC1 through PI3K-AKT signaling and is upregulated in OS. In the present study, we found that miR-342-5p inhibits Wnt7b expression via direct binding to Wnt7b 3'-UTR. miR-342-5p overexpression remarkably suppressed the viability and invasion while enhanced the apoptosis of OS cells; meanwhile, Wnt7b, β-catenin, c-myc, and cyclin D1 proteins were reduced while E-cadherin protein showed to be increased. Consistent with its expression pattern, Wnt7b exerted oncogenic effects on OS cells. Wnt7b could significantly attenuate the impacts of miR-342-5p. In conclusion, we demonstrated a miR-342-5p/Wnt7b axis that regulates the capacity of OS cells to proliferate and to invade through Wnt/β-catenin signaling. The miR-342-5p/Wnt7b axis might be novel targets for OS targeted therapy, which needs further in vivo and clinical investigations.Entities:
Keywords: Osteosarcoma (OS); Wnt/β-catenin signaling; Wnt7b; miR-342-5p
Year: 2019 PMID: 31601147 PMCID: PMC6927707 DOI: 10.1080/15384101.2019.1676087
Source DB: PubMed Journal: Cell Cycle ISSN: 1551-4005 Impact factor: 4.534