The aim of the study was to evaluate the effects of synuclein-γ (SNCG) silencing on gastric cancer SGC7901 cells and to elucidate the associated mechanisms. pGCSIL-lentiviral siRNA targeting of the SNCG gene was employed to inhibit SNCG expression. Several experiments such as quantitative real-time PCR, Western blotting, MTT, colony formation, migration assay, and flow cytometry were performed to investigate the biological behavior of infected SGC7901 cells. BALB/c nude mice were used as tumor xenograft models to assess the effects of SNCG silencing on tumor growth. Western blot analysis was carried out to determine the relative levels of AKT, p-AKT, ERK, and p-ERK expression. Our results showed that SNCG was overexpressed in SGC7901 cells as compared to normal gastric mucosal epithelial cells. SGC7901 cells transfected with SNCG siRNA demonstrated significantly decreased gastric cancer growth (p < 0.01), reduced cell migration, cell cycle arrest in the G0/G1 phase, promoted tumor cell apoptosis (p < 0.01), and inhibited tumorigenesis in xenograft animal models. Western blot analysis indicated that the protein levels of p-AKT and p-ERK were much lower in the SNCG siRNA group than in the control groups. The results of the present study suggest that SNCG siRNA plays a significant role in the proliferation, migration, and tumorigenesis of gastric cancer by downregulating the phosphorylation of AKT and ERK. RNA interference-mediated silencing of SNCG may provide an opportunity to develop a novel treatment strategy for gastric cancer.

Role of circ-FNTA in the progression of bladder cancer (BCa) and its underlying mechanism were investigated. circ-FNTA level in BCa tissues and cell lines was detected. The prognostic potential of circ-FNTA was assessed by Kaplan-Meier methods and the proliferative and invasive abilities of BCa influenced by circ-FNTA were explored. Through dual-luciferase reporter gene assay, miRNA-451a, the target of circ-FNTA and the target gene of miRNA-451a, S1PR3 were determined. circ-FNTA was upregulated in BCa, especially in invasive BCa. High level of circ-FNTA indicated worse prognosis in BCa patients. Silence of circ-FNTA attenuated the proliferative and invasive abilities of T24 and UM-UC-3 cells. miRNA-451a was verified to be the target of circ-FNTA, which was downregulated in BCa cells. circ-FNTA negatively regulated the expression level of miRNA-451a. Moreover, S1PR3 was the downstream gene of miRNA-451a. Overexpression of miRNA-451a downregulated S1PR3 level in BCa cells. circ-FNTA accelerates the proliferative and invasive abilities of BCa through targeting miRNA-451a/S1PR3 axis, and indicates a poor prognosis of BCa patients.

To investigate the effect of Kim-1 on 786-0 cells in vivo and in vitro, several experiments such as quantitative real-time PCR, Western blot, MTT, colony formation, and flow cytometry were performed to evaluate the biological behavior of 786-0 cells treated with Kim-1 siRNA. Furthermore, the tumor xenograft model was applied to BALB/c nude mice to assess the effect of Kim-1 silencing. Lentivirus-mediated RNAi effectively silenced Kim-1 in 786-0 cells. Kim-1 knockdown significantly inhibited the proliferation and colony formation ability of 786-0 cells (p < 0.01). The cell cycle of 786-0 cells was arrested in the G0/G1 phase (p < 0.01). Early and late apoptosis were significantly increased in the Kim-1 siRNA cells (p < 0.01). In addition, growth of 786-0 cells was significantly inhibited in the Kim-1-silenced mice. In conclusion, knockdown of Kim-1 inhibits the growth of 786-0 cells in vitro and in vivo, indicating that Kim-1 could be used as a potential target for clear cell renal cell carcinoma therapy.

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