| Literature DB >> 33462751 |
Yang Sun1, Wei Nie2, Bo Qiu3, Xiangjun Guo3, Jian Zhang3, Jianming Wei3.
Abstract
MicroRNA-17 (miR-17) was reported to promote cell proliferation and migration of various types of cancers. However, the mechanism remains unclear. This present study was designed to explore the potential mechanism. Downregulation of miR-17 in CAL-27 cells was performed by transfecting anti-miR-27 plasmids. Xenograft tumor model was carried out to detect the effect of inhibition of microRNA-17 on tongue squamous carcinoma growth. MiR-17 inhibition promotes cisplatin-induced apoptosis via regulating the expression of apoptotic molecules. MiR-17 inhibition promotes cisplatin-induced autophagy of CAL-27 cells. Mechanically, miR-17 inhibition promotes apoptosis and autophagy through STAT3 signaling pathway. Xenograft tumor model showed that miR-17 inhibition attenuates tongue squamous carcinoma growth and promotes tongue squamous carcinoma cell apoptosis in vivo. MiR-17 inhibition enhances cisplatin-induced apoptosis of human tongue squamous carcinoma cell. Our study supplies the evidence that miR-17 may serve as the potential target for human tongue squamous carcinoma treatment.Entities:
Keywords: Apoptosis; Autophagy; Cisplatin; Tongue squamous carcinoma; miR-17
Mesh:
Substances:
Year: 2021 PMID: 33462751 DOI: 10.1007/s10863-020-09869-x
Source DB: PubMed Journal: J Bioenerg Biomembr ISSN: 0145-479X Impact factor: 2.945