PURPOSE: Breast cancer is one of the leading causes of mortality in women across the globe. Herein, the role and therapeutic implications of miR-322 were investigated in breast cancer. METHODS: An array of breast cancer cell lines and a normal cell line were used in this study. The expression of miR-322 was determined by quantitative realtime polymerase chain reaction (qRT-PCR). Lipofectamine 2000 reagent was used to perform transfections and MTT assay was used to determine the cell viability. DAPI and annexin V/propidium iodide (PI) assays were used to detect apoptosis. Wound healing and transwell assays were used to monitor cell migration and invasion, respectively. Protein expression was determined by western blot analysis. RESULTS: The expression of miR-322 was found to be remarkably suppressed in breast cancer cells. Overexpression of miR-322 led to considerable decline in the proliferation rate and colony formation of the MCF7 breast cancer cells due to induction of apoptosis. The overexpression of miR-322 caused a significant increase in Bax and decrease in Bcl-2 expression and also enhanced the sensitivity of MCF7 cells to cisplatin and decreased their migration and invasive potential. The TargetScan analysis showed NF-kB1 to be the target of miR-322. Additionally, NF-kB1 was remarkably upregulated in all the breast cancer cells. However, miR-322 overexpression resulted in depletion of NF-kB1 expression in MCF7 cells. Silencing of NF-kB1 also decreased the proliferation rate and colony formation of the MCF7 cells. CONCLUSION: To conclude, miR-322 may exhibit therapeutic implications in breast cancer treatment and warrants further investigation.
PURPOSE:Breast cancer is one of the leading causes of mortality in women across the globe. Herein, the role and therapeutic implications of miR-322 were investigated in breast cancer. METHODS: An array of breast cancer cell lines and a normal cell line were used in this study. The expression of miR-322 was determined by quantitative realtime polymerase chain reaction (qRT-PCR). Lipofectamine 2000 reagent was used to perform transfections and MTT assay was used to determine the cell viability. DAPI and annexin V/propidium iodide (PI) assays were used to detect apoptosis. Wound healing and transwell assays were used to monitor cell migration and invasion, respectively. Protein expression was determined by western blot analysis. RESULTS: The expression of miR-322 was found to be remarkably suppressed in breast cancer cells. Overexpression of miR-322 led to considerable decline in the proliferation rate and colony formation of the MCF7breast cancer cells due to induction of apoptosis. The overexpression of miR-322 caused a significant increase in Bax and decrease in Bcl-2 expression and also enhanced the sensitivity of MCF7 cells to cisplatin and decreased their migration and invasive potential. The TargetScan analysis showed NF-kB1 to be the target of miR-322. Additionally, NF-kB1 was remarkably upregulated in all the breast cancer cells. However, miR-322 overexpression resulted in depletion of NF-kB1 expression in MCF7 cells. Silencing of NF-kB1 also decreased the proliferation rate and colony formation of the MCF7 cells. CONCLUSION: To conclude, miR-322 may exhibit therapeutic implications in breast cancer treatment and warrants further investigation.