Yunfeng Zhou

MicroRNA-133 inhibits cell proliferation, migration and invasion by targeting epidermal growth factor receptor and its downstream effector proteins in bladder cancer

Abstract Objective. MicroRNA-133a (miR-133a) and microRNA-133b (miR-133b) are located on chromosome 18 in the same bicistronic unit. Recently, they have been commonly identified as being down-regulated in various human malignancies, such as bladder cancer, pancreatic ductal adenocarcinoma, oesophageal squamous cell carcinoma of the tongue, and hepatocellular and lung carcinomas. The present study examined the effects of miR-133a and miR-133b in bladder cancer T24 and EJ cells. Material and methods. After transfection of miR-133a and miR-133b, the expression of miR-133a/b was assessed, and a cell viability assay, cell migration assay, cell invasion assay, luciferase assay and Western blot were conducted in bladder cancer T24 and EJ cells. Results. Both miR-133a and miR-133b were found to inhibit cell proliferation, migration and invasion in T24 and EJ cells. The first evidence was provided that miR-133a and miR-133b may directly target the epidermal growth factor receptor in bladder cancer. Conclusions. This study provided the first glimpse of the functional role of miR-133 in bladder cancer T24 and EJ cells. The results may increase our knowledge on the molecular basis of progression and provide potential therapy for bladder cancer.

MicroRNA-143 inhibits cell migration and invasion by targeting matrix metalloproteinase 13 in prostate cancer.

MicroRN-143 (miR‑143) has been previously reported to be downregulated in specific types of cancer, including colorectal, bladder, oral squamous cell, pituitary, cervical, nasopharyngeal, lymphoma and prostate cancer. In the present study, the effects of miR-143 on prostate cancer cell migration and invasion were examined. Following transfection with miR-143, miR-143 expression, cell migration and invasion assays, luciferase assay and western blot analysis were conducted in prostate cancer cell lines. The results indicated that miR-143 inhibits cell migration and invasion in DU145 and PC-3 cells. In addition, to the best of our knowledge, miR-143 was reported for the first time to directly target matrix metalloproteinase 13 (MMP-13) in prostate cancer. The results of the present study demonstrated that miR-143 suppresses cell migration and invasion by targeting MMP-13 in prostate cancer cell lines. These results indicated that miR-143 may be suitable for the development of novel molecular markers and therapeutic approaches to inhibit metastasis in prostate cancer.

microRNA‑99a inhibiting cell proliferation, migration and invasion by targeting fibroblast growth factor receptor 3 in bladder cancer

The expression of microRNA-99a (miRNA-99a) has been investigated in a number of human cancers. It has been reported to be downregulated in several types of cancer, including ovarian carcinoma, squamous cell carcinoma of the tongue, squamous cell lung carcinoma, hepatocellular carcinoma, bladder cancer, prostate cancer and childhood adrenocortical tumors. In the present study, the effects of miRNA-99a on bladder cancer cell proliferation, migration and invasion were examined. Following transfection of miRNA-99a, cell viability, cell migration assay, cell invasion, western blot analysis and luciferase assays were conducted in bladder cancer cell lines. It was found that miRNA-99a inhibits cell proliferation, migration and invasion in T24 and EJ cells. Additionally, this study provided the first evidence that miRNA-99a is likely to directly target fibroblast growth factor receptor 3 in bladder cancer. The study provided evidence that miRNA-99a suppresses cell proliferation, migration and invasion by targeting growth factor receptor 3 in bladder cancer cell lines. These results indicated that it could be investigated as a target for therapeutic drugs designed to treat bladder cancer.

microRNA-133b downregulation and inhibition of cell proliferation, migration and invasion by targeting matrix metallopeptidase‑9 in renal cell carcinoma

microRNA (miRNA)-133b has been revealed to be downregulated in head and neck/oral, bladder, human non-small cell lung, colorectal and esophageal squamous cell cancer. The present study examined the expression of miR-133b in renal cell carcinoma (RCC) cell lines and the effects of miRNA-133b on RCC cell proliferation, migration and invasion. Quantitative polymerase chain reaction was used to detect the expression of miR-133b in RCC cell lines. Following transfection of miR-133b, the expression of miR-133b was examined and a cell viability assay, cell migration assay, cell invasion assay, western blot analysis and luciferase assay were conducted in RCC cell lines. The present study revealed that miRNA‑133b was downregulated and inhibited cell proliferation, migration and invasion in 786-O and A498 cells. In addition, to the best of our knowledge, the present study provided the first evidence that miRNA-133b may directly target matrix metallopeptidase 9 (MMP-9) in RCC. The present study also provided evidence that miRNA-133b suppresses cell proliferation, migration and invasion by targeting MMP-9 in RCC cell lines. These results suggested that miRNA-133b may be used for the development of novel molecular markers and therapeutic approaches to inhibit the metastasis of RCC.

microRNA‑145 inhibits cell proliferation, migration and invasion by targeting matrix metallopeptidase-11 in renal cell carcinoma

microRNA‑145 (miR‑145) has been reported to be frequently downregulated in various types of cancer, including renal, prostate, bladder, lung and colon cancer, as well as B‑cell malignancies. The present study examined the effects of miR‑145 on the cell proliferation, migration and invasion of renal cell carcinoma (RCC). Following transfection of miR‑145, an MTT, cell migration, cell invasion and luciferase assays, and western blot analysis were conducted in RCC cell lines. The present study demonstrated that miR‑145 inhibited cell proliferation, migration and invasion in 786‑O and A498 cells. The present study also demonstrated for the first time, to the best of our knowledge, that miR‑145 may directly target matrix metallopeptidase‑11 (MMP‑11) in RCC. miR‑145 was demonstrated to suppress cell proliferation, migration and invasion by targeting MMP‑11 in RCC cell lines. These results suggested that it may be investigated as a predictive marker for the early detection of tumor metastasis and for targeting therapeutic drugs to inhibit the invasion of RCC.

Upregulation of microRNA-204 inhibits cell proliferation, migration and invasion in human renal cell carcinoma cells by downregulating SOX4

MicroRNA-204 (miR-204) has been reported to be frequently downregulated in various types of cancer, including renal, brain, ovary, hematological and colon cancer. The present study, investigated the effects of miR‑204 on renal cell carcinoma. Following transfection of miR‑204, an MTT assay, cell migration assay, cell invasion assay, western blot analysis and luciferase assay were performed in renal cell carcinoma cell lines. It was demonstrated that miR‑204 inhibits cell proliferation, migration and invasion in 786‑O and A498 cells. To the best of our knowledge, this study is the first to demonstrate that miR‑204 directly targets SOX4 in renal cell carcinoma. These results suggested that miR-204 may have value as a marker for the early detection of tumor metastasis and a therapeutic target preventing the invasion of renal cell carcinoma.

MicroRNA-497 targets hepatoma-derived growth factor and suppresses human prostate cancer cell motility.

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.

microRNA‑99a inhibits cell proliferation, colony formation ability, migration and invasion by targeting fibroblast growth factor receptor 3 in prostate cancer

microRNA‑99a (miR‑99a) was reported to be among the most frequently downregulated miRNAs in numerous types of human cancers, including prostate, bladder, hepatocellular and ovarian carcinoma, squamous cell carcinoma of the tongue, squamous cell lung carcinoma as well as childhood adrenocortical tumors. The aim of the present study was to determine the effects of miRNA‑99a on cell proliferation, colony formation ability, migration and invasion in prostate cancer. Following transfection with miRNA‑99a, cell viability, colony formation, cell migration and cell invasion assays were performed on prostate cancer cell lines, as well as western blot analysis and luciferase assays. miRNA‑99a inhibited cell proliferation, colony formation ability, migration and invasion in DU145 and PC‑3 cells, therefore indicating that miRNA‑99a may have a tumor suppressive role in prostate cancer. In addition, the present study provided the first evidence that the mechanism of action of miRNA‑99a may proceed by directly targeting fibroblast growth factor receptor 3 in prostate cancer. In conclusion, the results of the present study suggested that miRNA‑99a may have potential use as a therapeutic target for the treatment of prostate cancer.

Association between single nucleotide polymorphisms in the XRCC1 gene and susceptibility to prostate cancer in Chinese men.

BACKGROUND Prostate cancer (Pca) is one of the most common complex and polygenic diseases in men. The X-ray repair complementing group 1 gene (XRCC1) is an important candidate in the pathogenesis of Pca. The purpose of this study was to evaluate the association between single nucleotide polymorphisms in the XRCC1 gene and susceptibility to Pca. MATERIALS AND METHODS XRCC1 gene polymorphisms and associations with susceptibility to Pca were investigated in 193 prostate patients and 188 cancer-free Chinese men. RESULTS The c.910A>G variant in the exon9 of XRCC1 gene could be detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and DNA sequencing methods. Significantly increased susceptibility to prostate cancer was noted in the homozygote comparison (GG versus AA: OR=2.95, 95% CI 1.46-5.42, χ2=12.36, P=0.001), heterozygote comparison (AG versus AA: OR=1.76, 95% CI 1.12-2.51, χ2=4.04, P=0.045), dominant model (GG/AG versus AA: OR=1.93, 95% CI 1.19-2.97, χ2=9.12, P=0.003), recessive model (GG versus AG+AA: OR=2.17, 95% CI 1.33-4.06, χ2=8.86, P=0.003) and with allele contrast (G versus A: OR=1.89, 95% CI 1.56-2.42, χ2=14.67, P<0.000). CONCLUSIONS These findings suggest that the c.910A>G polymorphism of the XRCC1 gene is associated with susceptibility to Pca in Chinese men, the G-allele conferring higher risk.