BACKGROUND: In the present study, we investigated the possible tumor suppressive effect of microRNA-107 (miR-107) in human breast cancer. METHODS: Gene expression of miR-107 in breast cancer cell lines and clinical breast tissues was evaluated by a quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). MiR-107 was stably overexpressed in MCF-7 and MDA-MB-231 cells via lentiviral transduction. Its role in regulating in vitro cancer proliferation, cell cycle, invasion and in vivo tumor growth was evaluated by MTT, flow cytometry, transwell and in vivo tumorigenicity assays, respectively. Association of miR-107 and its downstream target, brain-derived neurotrophic factor (BDNF), was evaluated by luciferase assay and qRT-PCR. BDNF was further upregulated in miR-107-overexpressed MCF-7 and MDA-MB-231 cells to evaluate its role in regulating breast cancer with respect to in vitro proliferation, cell cycle and invasion. RESULTS: MiR-107 was markedly downregulated in both breast cancer cell lines and breast tumors. MiR-107 overexpression was markedly suppressed with respect to in vitro breast cancer proliferation, cell cycle progression and invasion, as well as with respect to in vivo development of breast cancer xenograft. BDNF was found to be the downstream target of miR-107 in breast cancer. BDNF upregulation functionally facilitated in vitro proliferation, cell cycle progression and invasion in miR-107-overexpressed breast cancer cells. CONCLUSIONS: MiR-107 is downregulated and has a tumor suppressive effect in breast cancer, likely through regulation via its inverted downstream target of BDNF.
BACKGROUND: In the present study, we investigated the possible tumor suppressive effect of microRNA-107 (miR-107) in humanbreast cancer. METHODS: Gene expression of miR-107 in breast cancer cell lines and clinical breast tissues was evaluated by a quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). MiR-107 was stably overexpressed in MCF-7 and MDA-MB-231 cells via lentiviral transduction. Its role in regulating in vitro cancer proliferation, cell cycle, invasion and in vivo tumor growth was evaluated by MTT, flow cytometry, transwell and in vivo tumorigenicity assays, respectively. Association of miR-107 and its downstream target, brain-derived neurotrophic factor (BDNF), was evaluated by luciferase assay and qRT-PCR. BDNF was further upregulated in miR-107-overexpressed MCF-7 and MDA-MB-231 cells to evaluate its role in regulating breast cancer with respect to in vitro proliferation, cell cycle and invasion. RESULTS:MiR-107 was markedly downregulated in both breast cancer cell lines and breast tumors. MiR-107 overexpression was markedly suppressed with respect to in vitro breast cancer proliferation, cell cycle progression and invasion, as well as with respect to in vivo development of breast cancer xenograft. BDNF was found to be the downstream target of miR-107 in breast cancer. BDNF upregulation functionally facilitated in vitro proliferation, cell cycle progression and invasion in miR-107-overexpressed breast cancer cells. CONCLUSIONS:MiR-107 is downregulated and has a tumor suppressive effect in breast cancer, likely through regulation via its inverted downstream target of BDNF.
Authors: Sara Donzelli; Elisa Milano; Magdalena Pruszko; Andrea Sacconi; Silvia Masciarelli; Ilaria Iosue; Elisa Melucci; Enzo Gallo; Irene Terrenato; Marcella Mottolese; Maciej Zylicz; Alicja Zylicz; Francesco Fazi; Giovanni Blandino; Giulia Fontemaggi Journal: Breast Cancer Res Date: 2018-06-19 Impact factor: 6.466