Effect of MicroRNA-766 Promotes Proliferation, Chemoresistance, Migration, and Invasion of Breast Cancer Cells.

INTRODUCTION: Breast cancer (BCa) remains the most common cancer in women worldwide. It has been shown that microRNAs (miRs) play essential roles in tumorigenesis and progression in many types of cancers, including BCa. We assessed the role of miR-766 on the proliferation, chemosensitivity, migration, and invasion of BCa cells. MATERIALS AND METHODS: The effect of miR-766 on the proliferation of MCF-7 and T47D BCa cells was evaluated using the MTT assay. The function of miR-766 on the migration and invasion of MCF-7 and T47D cells was examined using Transwell migration and Matrigel invasion assays. Protein expression was evaluated by Western blot. The role of miR-766 on 5-fluorouracil-induced apoptosis in MCF-7 and T47D cells was determined using the Caspase-Glo3/7 assay. A subcutaneous tumor xenograft was performed to examine the effect of miR-766 on tumor growth in vivo. RESULTS: Upregulation of miR-766 improved the proliferation, invasion, and migration of BCa cells. Furthermore, miR-766 reduced the sensitivity of MCF-7 and T47D cells to 5-fluorouracil treatment. The tumor xenograft experiment showed that miR-766 promoted BCa growth in vivo. miR-766 decreased 5-flurouracil-induced apoptosis by regulation of BAX and Bcl-2 expression. miR-766 also affected the epithelial-mesenchymal transition by altering E-cadherin, N-cadherin, SNAIL, and vimentin expression in MCF-7 and T47D cells. Further study showed that the expression of phosphatase and tensin homolog and phosphorylated AKT in MCF-7 and T47D cells had changed after aberrant expression of miR-766. CONCLUSION: miR-766 displayed important roles in tumorigenesis and progression in BCa cells and might act as a potential biomarker to predict the chemotherapy response and progression in BCa.

MicroRNA-135a promotes proliferation, migration, invasion and induces chemoresistance of endometrial cancer cells.

AIMS: MicroRNAs play essential roles in tumorigenesis and progression in various cancers including endometrial cancer. Here we assessed the role of miR-135a on proliferation, chemosensitivity, migration and invasion of endometrial cancer cells. METHODS: WST-1 assay was performed to examine the proliferation of HEC-1-B and ISHIKAWA endometrial cancer cells with altered expression of miR-135a, with or without cisplatin treatment. Transwell migration and matrigel invasion assays were used to assess the migration and invasion of endometrial cancer cells. The Caspase-Glo3/7 assay was used to examine the effect of miR-135a on cisplatin-induced apoptosis of endometrial cancer cells. The dual-luciferase reporter assay was conducted to validate the putative binding site. RESULTS: Upregulation of miR-135a improved the proliferation, and promoted migration and invasion of endometrial cancer cells. Furthermore, miR-135a decreased the sensitivity of HEC-1-B and ISHIKAWA cells after cisplatin treatment. The cisplatin-induced apoptosis in endometrial cancer cells was inhibited by miR-135a by regulation of BAX and Bcl-2 expression. Meanwhile, miR-135a could regulate epithelial to mesenchymal transition (EMT) by altering the expression of E-cadherin, N-cadherin, snail and Vimentin in endometrial cancer cells. Further study showed that the expression levels of PTEN and p-AKT in endometrial cancer cells were changed after aberrant expression of miR-135a. CONCLUSION: MiR-135a played important roles in tumorigenesis and disease progression of endometrial cancer by regulating proliferation and chemosensitivy of endometrial cancer cells by targeting AKT signaling pathway. Our study indicates that miR-135a might act as a potential biomarker to predict chemotherapy response and prognosis in endometrial cancer.

MicroRNA-498 promotes proliferation, migration, and invasion of prostate cancer cells and decreases radiation sensitivity by targeting PTEN.

Prostate cancer (PCa) remains the secondary highest cause of cancer-related death in the United States in men. It has been reported that microRNAs can serve as key regulators in tumor development and progression in various cancers including PCa. In this study, we examined the effect of miR-498 on proliferation, radiosensitivity, invasion, and migration of PCa cells. The proliferation of LNCaP and DU-145 PCa cells with altered expression of miR-498 was evaluated by MTT assay. The invasion and migration of LNCaP and DU-145 PCa cells were assess by matrigel invasion assay and transwell migration assay. The protein expression level in PCa cells was examined by western blot. The function of miR-498 on radiation-induced apoptosis in LNCaP and DU-145 PCa cells was detected by Caspase-Glo3/7 assay. Forced expression of miR-498 improved the proliferation, invasion and migration in PCa cells. Furthermore, miR-498 decreased the sensitivity of PCa cells after ionizing radiation treatment. MiR-498 reduced the radiation-induced apoptosis in PCa cells by regulation of BAX and Bcl-2 expression. Meanwhile, miR-498 altered the expression of E-cadherin, N-cadherin, snail, and Vimentin in both LNCaP and DU-145 PCa cells and regulated epithelial to mesenchymal transition (EMT). Further study showed that aberrant expression of miR-498 changed the expression levels of phosphatase and tensin homolog and p-AKT in LNCaP and DU-145 PCa cells. In a summary, miR-498 displayed important roles in tumor development and progression in PCa cells, and might act as a potential prognostic biomarker and predict radiotherapy response in PCa.