Furthermore, previous studies also revealed that miR-320c could inhibit the motility of hepatocellular cancer www.selleckchem.com/products/bmn-673.html and regulate the resistance of pancreatic cancer cells to gemcitabine [20,21]. However, owing to unique genetic background in different types of cancer, the biological function of miR-320c in bladder cancer was not well elucidated. Therefore, this is the first study to determine the functional role of miR-320c in bladder cancer. Considering both of our tissue samples and cell lines are from patients with muscle-invasive bladder
cancer, the outcome of this study is probably more meaningful in muscle-invasive or recurrent cancer. Our study illustrated that miR-320c was down-regulated in bladder cancer tissues compared with normal adjacent tissues, though the sample size was relatively small. Similar result was detected in 4 bladder cancer cell lines compared with non-tumor urothelial cell line SV-HUC-1, which further strengthened the conclusion that miR-320c was down-regulated
in bladder cancer. A gain-of- function study was further conducted in bladder cancer cell lines. When both UM-UC-3 and T24 cells were transfected with miR-320c, we observed {Selleck Anti-infection Compound Library|Selleck Antiinfection Compound Library|Selleck Anti-infection Compound Library|Selleck Antiinfection Compound Library|Selleckchem Anti-infection Compound Library|Selleckchem Antiinfection Compound Library|Selleckchem Anti-infection Compound Library|Selleckchem Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|buy Anti-infection Compound Library|Anti-infection Compound Library ic50|Anti-infection Compound Library price|Anti-infection Compound Library cost|Anti-infection Compound Library solubility dmso|Anti-infection Compound Library purchase|Anti-infection Compound Library manufacturer|Anti-infection Compound Library research buy|Anti-infection Compound Library order|Anti-infection Compound Library mouse|Anti-infection Compound Library chemical structure|Anti-infection Compound Library mw|Anti-infection Compound Library molecular weight|Anti-infection Compound Library datasheet|Anti-infection Compound Library supplier|Anti-infection Compound Library in vitro|Anti-infection Compound Library cell line|Anti-infection Compound Library concentration|Anti-infection Compound Library nmr|Anti-infection Compound Library in vivo|Anti-infection Compound Library clinical trial|Anti-infection Compound Library cell assay|Anti-infection Compound Library screening|Anti-infection Compound Library high throughput|buy Antiinfection Compound Library|Antiinfection Compound Library ic50|Antiinfection Compound Library price|Antiinfection Compound Library cost|Antiinfection Compound Library solubility dmso|Antiinfection Compound Library purchase|Antiinfection Compound Library manufacturer|Antiinfection Compound Library research buy|Antiinfection Compound Library order|Antiinfection Compound Library chemical structure|Antiinfection Compound Library datasheet|Antiinfection Compound Library supplier|Antiinfection Compound Library in vitro|Antiinfection Compound Library cell line|Antiinfection Compound Library concentration|Antiinfection Compound Library clinical trial|Antiinfection Compound Library cell assay|Antiinfection Compound Library screening|Antiinfection Compound Library high throughput|Anti-infection Compound high throughput screening| that miR-320c could suppress bladder cancer cell viability and inhibit clone formation. In addition, flow
cytometry indicated that miR-320c could trigger G1-phase arrest, which could be the potential mechanism of miR-320c-regulated proliferation inhibition. Moreover, cell motility assay demonstrated that over-expression of miR-320c impaired bladder cancer cells migration and invasion ability. To elucidate the possible mechanism responsible for the anticancer behaviors triggered by miR-320c, we conducted a computerized analysis for the potential target. Therefore, we identified CDK6 as a new target of miR-320. A previous study illustrated that CDK6 was over-expressed Methane monooxygenase in bladder cancer tissue [26]. In our present study, similar expression pattern of CDK6 was observed in the human bladder cancer cell lines, which suggested the oncogenic role of CDK6 in bladder cancer. PCR and Western blot study indicated that miR-320c could dramatically inhibit CDK6 expression and luciferase assay further confirmed that CDK6 was a downstream target of miR-320c via directly binding to the 3′-UTR. To better verify the function of miR-320c, the antisense inhibitor (miR-320c inhibitor) experiments were performed. We confirmed that miR-320c-Inh could reverse the effects to over-expression of miR-320c.
