Objective To explore the molecular mechanism of microRNA-26b(miR-26b)inhibiting the malignant biological behavior of MCF-7 breast cancer cells through MALAT-1.Methods MCF-7 breast cancer cell line was transduced with lentivirus-based vectors LV-miR-26b-ctrl and LV-miR-26b,and expressions of MALAT-1,miR-26a and miR-26b were measured by RT-PCR.The colony formation assay,CCK-8 assay,soft agar colony formation assay,scratch assay,and Transwell invasion assay were performed to detect the proliferation ability,in vitro tumorigenic capability,and migration and invasion abilities,respectively.Results The optical density values of MCF-7 cells at 24 h,48 h,72 h and 96 h in the E2 group and the Mock group were compared via the repeated measures analysis of variance,which demonstrated that they were different among the time points(P＜0.05)and between the two groups(P＜0.05),and that the proliferation ability of cells at 72 h and 96 h in the E2 group was higher than that in the Mock group(P＜0.05).There were differences in the change trends of the optical density values between the two groups(P＜0.05).Compared with the Mock group,the expression of MALAT-1 in the E2 group was higher(P＜0.05),and the expressions of miR-26a and miR-26b were lower(P＜0.05).Compared with the miR-26b low-expression group,the position of the survival curve of patients with breast cancer was higher in the miR-26b high-expression group,indicating a lower risk of death(P＜0.05).Compared with the miR-26a low-expression group,the position of the survival curve of patients with breast cancer was lower in the miR-26a high-expression group(P＜0.05).However,the risk of death was not significantly different between the two groups when including miR-26a as an independent prognostic factor in the Cox regression model(P＞0.05).The expression of MALAT-1 in breast cancer cells of the LV-miR-26b-ctrl/E2 was higher than that in the LV-miR-26b-ctrl group(P＜0.05),while the expression of MALAT-1 in breast cancer cells of the LV-miR-26b/E2 group was lower than that in the LV-miR-26b-ctrl/E2(P＜0.05).The optical density values of cells at 24 h,48 h,72 h and 96 h in the LV-miR-26b-ctrl group,LV-miR-26b-ctrl/E2 group,and LV-miR-26b/E2 group were compared via the repeated measures analysis of variance,and the results showed that they were different among the time points(P＜0.05)and among the groups(P＜0.05).The proliferation ability of cells at 72 h and 96 h in the LV-miR-26b-ctrl/E2 group was higher than that in the LV-miR-26b-ctrl group(P＜0.05),and the proliferation ability of cells at 72 h and 96 h in the LV-miR-26b/E2 group was lower than that in the LV-miR-26b-ctrl/E2 group(P＜0.05).There were differences in the change trends of the optical density values of cells among the groups(P＜0.05).After E2 treatment,the proliferation ability and in vitro tumorigenic capability of cancer cells in the LV-miR-26b-ctrl group were enhanced.Compared with the LV-miR-26b-ctrl/E2 group,the proliferation ability and in vitro tumorigenic capability of cancer cells in the LV-miR-26b/E2 group were weakened.At 24 h,the gap in the scratch assay in the LV-miR-26b-ctrl/E2 group was narrower than that in the LV-miR-26b-ctrl group,while the gap in the scratch assay in the LV-miR-26b/E2 group was wider than that in the LV-miR-26b-ctrl/E2.The number of breast cancer cells in the bottom chamber of the Transwell in the LV-miR-26b-ctrl/E2 group was higher than that in the LV-miR-26b-ctrl group,whereas that in the LV-miR-26b/E2 group was lower compared with the LV-miR-26b-ctrl/E2 group.Conclusions Down-regulation of MALAT-1 may be one of the mechanisms underlying the role of miR-26b in inhibiting the malignant biological behavior of MCF-7 breast cancer cells,and miR-26b holds promise as a target for breast cancer therapy.
breast cancermicroRNA-26bMALAT-1estradiollncRNAinvasionmetastasis
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