title: miR‑205 suppresses cell proliferation, invasion, and metastasis via regulation of the PTEN/AKT pathway in renal cell carcinoma.
abstract: The present study aimed to determine the importance of microRNA‑205 (miR‑205) in the proliferation, apoptosis, invasion and metastasis of renal cell carcinoma (RCC) cells and the underlying molecular mechanisms. Reverse transcription‑polymerase chain reaction was used to quantify the expression levels of miR‑205 in RCC tissue, normal tissue adjacent to carcinoma, RCC cells and normal renal cells. It was determined that the expression levels of miR‑205 in RCC tissue and cells were reduced compared with those in normal tissue and renal cells. miR‑205 mimics and the negative control were prepared and transfected into RCC cells. Cell viability and apoptosis were investigated using methyl thiazolyl tetrazolium assay and Annexin V‑fluorescein isothiocyanate/propidium iodide staining, respectively. Cell migration and invasion were evaluated with Transwell assays. The protein expression levels of E2F transcription factor 1 (E2F1), B‑cell lymphoma‑2 (Bcl‑2), E‑cadherin, vimentin, phosphatase and tensin homolog (PTEN) and phosphorylated AKT serine/threonine kinase 1 (p‑AKT) were determined with western blot analysis. It was revealed that miR‑205 promoted the apoptosis of RCC cells and suppressed their proliferation, metastasis and invasion compared with the negative control. The expression levels of E2F1, Bcl‑2, vimentin and p‑AKT were downregulated compared with the negative control. The expression levels of E‑cadherin and PTEN were upregulated in the cells transfected with miR‑205 mimics compared with the negative control group. Therefore, it was concluded that miR‑205 suppressed cell proliferation, invasion, and metastasis in RCC cells via regulation of the PTEN/AKT signaling pathway. The present study may contribute to future miRNA‑based RCC therapy.
authors: Department of Urology, First Affliated Hospital of Xiamen University, Xiamen, Fujian 361003, P.R. China.
authors: Huiqiang
authors: H
authors: Wang
authors: Department of Urology, First Affliated Hospital of Xiamen University, Xiamen, Fujian 361003, P.R. China.
authors: Bin
authors: B
authors: Chen
authors: Department of Urology, First Affliated Hospital of Xiamen University, Xiamen, Fujian 361003, P.R. China.
authors: Bo
authors: B
authors: Duan
authors: Department of Urology, First Affliated Hospital of Xiamen University, Xiamen, Fujian 361003, P.R. China.
authors: Jiaxin
authors: J
authors: Zheng
authors: Department of Breast Surgery, First Affliated Hospital of Xiamen University, Xiamen, Fujian 361003, P.R. China.
authors: Xinyi
authors: X
authors: Wu
mesh_terms: D002292:Carcinoma, Renal Cell / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007668:Kidney / Q000378:metabolism / Q000473:pathology*; D007680:Kidney Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D035683:MicroRNAs / Q000235:genetics*; D009361:Neoplasm Invasiveness / Q000235:genetics / Q000473:pathology; D009362:Neoplasm Metastasis / Q000235:genetics / Q000473:pathology; D051059:PTEN Phosphohydrolase / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D035683:MicroRNAs; D051059:PTEN Phosphohydrolase; D051057:Proto-Oncogene Proteins c-akt; C534425:MIR205, human; C494929:PTEN protein, human