MicroRNA-504 functions as a tumor suppressor in oral squamous cell carcinoma through inhibiting cell proliferation, migration and invasion by targeting CDK6.

MicroRNA (miRNA), as tumor suppressor or oncogene, is involved in the regulation of tumor development. However, the role of miRNA in human oral squamous cell carcinoma (OSCC) is less well understood. In our previous studies, we have successfully established a Chinese hamster oral squamous cell carcinoma animal model and constructed a miRNA differential expression profile, and screened out the abnormal expressed gene (miR-504). The purpose of this study was to investigate the regulatory mechanism of miR-504 in human OSCC cells and to elucidate its new target genes. CCK-8 assay, colony formation assay, transwell migration and invasion assay were used to test the cell proliferation, cell growth, cell migration and cell invasion abilities of the miR-504 mimics group, respectively. Flow cytometry was used to detect the apoptotic ability. In order to verify the direct target of miR-504, we used the dual luciferase reporting system for detection. The expressions of RNA and proteins were detected by qRT-PCR and western blotting. The results of our study showed that miR-504 expression was down-regulated in OSCC animal tissue samples. In human OSCC cell lines, miR-504 over-expression significantly inhibited cell proliferation, migration and invasion. The dual luciferase reporting system confirmed that CDK6 was a direct target of miR-504 and that miR-504 expression inhibited CDK6 expression. In addition, the over-expression of miR-504 in OSCC cells could significantly inhibit the expression of cell cycle-related proteins (E2F1, Cyclin D1), but the expression of p21 was significantly increased. The results of this study suggest that miR-504 may be a new therapeutic target for OSCC.

Wang X ，Chang K ，Gao J ，Wei J ，Xu G ，Xiao L ，Song G ... -  《-》

Low expression of lncRNA MEG3 promotes the progression of oral squamous cell carcinoma by targeting miR-21.

Zhang LL ，Hu D ，Zou LH 《-》

MiR-34a inhibits the proliferation, migration, and invasion of oral squamous cell carcinoma by directly targeting SATB2.

In various kinds of carcinomas, the special AT-rich sequence-binding protein 2 (SATB2) with its atypical expression promotes the metastasis and progression of the tumor, though in the oral squamous cell carcinoma (OSCC) its inherent mechanism and the status of SATB2 remain unclear. The role played by the SATB2 expression in the OSCC cell lines and tissue samples in the target of miR-34a downstream is the intended endeavor of this study. In te OSCCs the miR-34a expression was determined by quantitative real-time polymerase chain reaction (q-PCR), while the SATB2 expression in the cell lines and tissue samples in OSCC was analyzed with the q-PCR and the western blot. Studies in both in vitro and in vivo of the effects of miR-34a on the initiation of OSCC were conducted. As a direct target of the miR-34a the SATB2 was verified with the luciferase reporter assay. In cases where the miR-34a levels were low, the SATB2 in OSCCs seemed to be overexpressed. Besides, both in the in vitro and in vivo a suppression of migration, invasion, and cell growth was caused by miR-34a by down regulating the SATB2 expression. The SATB2 being a direct target of miR-34a was confirmed by the cotransfection of miR-34a mimics specifically the decrease in the expression of luciferase of SATB2-3'UTR-wt reporter. As a whole, our study confirmed the inhibition of miR-34a in the invasion, proliferation, and migration of the OSCCs, playing a potential tumor suppressor role with SATB2 as its downstream target.

Ge X ，Gao J ，Sun QW ，Wang CX ，Deng W ，Mao GY ，Li HQ ，Guo SS ，Cheng J ，Wu YN ，Ye JH ... -  《-》

MiR-590-5p regulates cell proliferation, apoptosis, migration and invasion in oral squamous cell carcinoma by targeting RECK.

Bao WW ，Shi YL ，Ma Y ，Qu XH ，Pang GM ，Yang L ... -  《-》

LncRNA GACAT1 targeting miRNA-149 regulates the molecular mechanism of proliferation, apoptosis and autophagy of oral squamous cell carcinoma cells.

Chen J ，Chen X ，Fu L ，Chen J ，Chen Y ，Liu F ... -  《Aging-US》