Mechanism of microRNA-138 in inhibiting invasion and migration of breast cancer by regulating epithelial mesenchymal transformation / 中国医师进修杂志

ABSTRACT

Objective To investigate the molecule mechanism of microRNA (miR)-138 in inhibiting invasion and migration of breast cancer by regulating epithelial mesenchymal transformation (EMT). Methods Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect expression of miR-138 after transfecting miR negative control simulacrum (miR-NC) and miR-138 simulacrum in human normal mammary epithelial cell (MCF-10A) and breast cancer cells (MCF-7 and MDA-MB-231) from July 2017 to June 2018. MTT method was used to detect the breast cancer cell activity. Cell scratch test and Transwell test were used to detect the breast cancer cell migration distance and invasion rate. RT-PCR was used to detect the expression of the EMT key molecules Vimentin, N-cadherin and E-cadherin after transfecting miR-138 simulacrum. Results The expression level of miR-138 in MCF-10A was significantly higher than that in MCF-7 and MDA-MB-231 (1.006 ± 0.009 vs. 0.324 ± 0.027 and 0.512 ± 0.068), and there was statistical difference (P<0.05);there was no statistical difference in the expression level of miR-138 between MCF-7 and MDA-MB-231 (P>0.05). The breast cancer cell viabilities of MCF-7 and MDA-MB-231 at third and fourth day after transfecting miR-138 simulacrum were significantly lower than those of transfecting miR-NC (MCF-7 0.514 ± 0.052 vs. 0.593 ± 0.061 and 0.643 ± 0.074 vs. 0.784 ± 0.081;MDA-MB-2310.552 ± 0.043 vs. 0.614 ± 0.063 and 0.673 ± 0.074 vs. 0.792 ± 0.077), and there were statistical differences (P<0.05). The breast cancer cell migration distances and invasion rates of MCF-7 and MDA-MB-231 after transfecting miR-138 simulacrum were significantly lower than those of transfecting miR-NC (MCF-7 0.572 ± 0.051 vs. 1.003 ± 0.012 and 0.624 ± 0.043 vs. 1.002 ± 0.007, MDA-MB-2310.472 ± 0.051 vs. 1.003 ± 0.095 and 0.573 ± 0.044 vs. 1.004 ± 0.091), and there were statistical differences (P<0.05). The expressions of Vimentin and N-cadherin mRNA in MCF-7 and MDA-MB-231 after transfecting miR-138 simulacrum were significantly lower than those of transfecting miR-NC, but the expression of E-cadherin mRNA was significantly increased, and there were statistical differences (P<0.05). Conclusions The expressions of miR-138 in both breast cancer cells decreased. Overexpression of miR-138 in breast cancer cell can inhibit proliferation, migration and invasion via regulating EMT.