Abstract. MicroRNA (miR)-429 has been frequently reported to be downregulated in various tumors, including renal cell carcinoma (RCC), nasopharyngeal carcinoma, Ehrlich ascites tumor cells, gastric cancer, non-small cell lung cancer and endometrial endometrioid carcinoma. The present study investigated the effects of miR-429 on human RCC A498 and 786-O cells. Following transfection of cells with miR-429 mimics and scrambled control, MTT, cell migration, cell invasion and luciferase assays were performed. In addition, western blotting was performed in order to assess the expression of specificity protein 1 (Sp1), which was predicted to be a target of miR-429 by TargetScan. The present results revealed that miR-429 inhibited cell proliferation, migration and invasion of 786-O and A498 cells. In addition, the present results demonstrated that miR-429 overexpression downregulated Sp1 protein expression, which provides evidence that miR-429 may directly target Sp1 in RCC. These results suggest that miR-429 may be investigated for use as a predictive marker for early detection of tumor metastasis and blocking RCC cells from becoming invasive.
MicroRNA-497 (miR-497) has been reported to be downregulated in certain types of cancer, including breast, gastric, endometrial, colorectal and prostate cancer as well as hepatocellular and nasopharyngeal carcinoma. The present study aimed to investigate the underlying mechanism of the tumor suppressor function of miR‑497 in prostate cancer. Following transfection with miR‑497, the DU145 and PC‑3 prostate cancer cell lines were subjected to Transwell migration and invasion assays, western blot analysis and a luciferase assay. It was revealed that miRNA‑497 inhibited the migration and invasion of prostate cancer cells. In addition, is was indicated that miRNA‑497 directly targets hepatoma‑derived growth factor (HDGF) in prostate cancer cells. These results suggested that restoration of miR‑497 and the resulting downregulation of HDFG may represent a promising therapeutic strategy for prostate cancer.
Abstract. Dysregulation of B7-H3 has been observed in a variety of types of human cancers. In the present study, the mRNA expression level of B7-H3 was analyzed in bladder cancer by performing semi-quantitative reverse transcription-polymerase chain reaction on clinical specimens from transitional cell carcinomas (TCCs) and their normal adjacent tissues (NATs).Immunohistochemical analysis was performed to compare the protein expression level of B7-H3 in TCCs and the paired NATs. The present study indicated that the B7-H3 mRNA expression level was significantly higher in the TCC samples compared with the paired NAT samples. Furthermore, immunohistochemical analyses indicated that the B7-H3 protein expression level was significantly upregulated in the TCC samples compared with in the paired NAT samples, indicating that B7-H3 dysregulation may be important in the progression of bladder cancer.
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