Background: Renal cell carcinoma (RCC) is one of the most common and malignant tumors in the urinary system. The aim of this research was to investigate the mechanism and clinical significance of miR-4461 in the RCC progression. Materials and Methods: Twenty-eight (28) paired RCC tissue samples and adjacent nontumor tissue samples, as well as RCC cell lines were used to measure the expression of miR-4461 and protein phosphatase 1 regulatory subunit 3C (PPP1R3C) transcript by real-time quantitative PCR. The target relationship between miR-4461 and PPP1R3C was predicted by TargetScan and further verified by dual-luciferase reporter gene assay and RNA pull-down assay. Cell Counting Kit-8 (CCK-8) assay and BrdU ELISA assay were performed to measure RCC cell viability and proliferation. In addition, caspase-3 activity assay and cell adhesion assay were implemented to measure RCC cell apoptosis and adhesion. Results: MiR-4461 was lowly expressed both in RCC tissues and cells, while upregulated PPP1R3C was tested in RCC tissues and cells. In addition, miR-4461 was validated to directly target PPP1R3C, thereby negatively regulating PPP1R3C. Particularly, miR-4461 exerted a clear inhibitory effect on the malignant phenotypes of RCC cells by binding and inhibiting PPP1R3C. Conclusion: MiR-4461, which served as a tumor suppressor, inhibited RCC progression by targeting and downregulating PPP1R3C.
Background: Renal cell carcinoma (RCC) is one of the most common and malignant tumors in the urinary system. The aim of this research was to investigate the mechanism and clinical significance of miR-4461 in the RCC progression. Materials and Methods: Twenty-eight (28) paired RCC tissue samples and adjacent nontumor tissue samples, as well as RCC cell lines were used to measure the expression of miR-4461 and protein phosphatase 1 regulatory subunit 3C (PPP1R3C) transcript by real-time quantitative PCR. The target relationship between miR-4461 and PPP1R3C was predicted by TargetScan and further verified by dual-luciferase reporter gene assay and RNA pull-down assay. Cell Counting Kit-8 (CCK-8) assay and BrdU ELISA assay were performed to measure RCC cell viability and proliferation. In addition, caspase-3 activity assay and cell adhesion assay were implemented to measure RCC cell apoptosis and adhesion. Results: MiR-4461 was lowly expressed both in RCC tissues and cells, while upregulated PPP1R3C was tested in RCC tissues and cells. In addition, miR-4461 was validated to directly target PPP1R3C, thereby negatively regulating PPP1R3C. Particularly, miR-4461 exerted a clear inhibitory effect on the malignant phenotypes of RCC cells by binding and inhibiting PPP1R3C. Conclusion: MiR-4461, which served as a tumor suppressor, inhibited RCC progression by targeting and downregulating PPP1R3C.