Objective To investigate the effects of microRNA-134 (miR-134) on the proliferation and apoptosis of non-small cell lung cancer (NSCLC) and its potential molecular mechanism.Methods Quantitative real-time fluorescent polymerase chain reaction (qRT-PCR) was used to detect the differences of miR-134 expression between 10 cases of lung cancer tissues and normal lung tissues,and between normal human lung epithelial cell line BEAS-2B and lung adenocarcinoma cell line A549.miR-NC and miR-134 mimic were transfected into A549 cells.The effect of miR-134 on proliferation of A549 cells was detected by methyl thiazolyl tetrazolium (MTT) and colony form experiment.Flow cytometry was used to determine the effect of miR-134 on A549 cells apoptosis.The effect of miR-134 on the expression of P53 protein was detected by Western blotting.Results The relative expressions of miR-134 in NSCLC tumor tissues and adjacent tissues were 0.429 ± 0.126 and 0.971 ±0.183 respectively,and the difference was statistically significant (t =7.742,P ＜0.001).The relative expressions of miR-134 in BEAS-2B cells and A549 cells were 1.013 ± 0.095 and 0.371 ± 0.068 respectively,and the difference was statistically significant (t =17.377,P ＜ 0.001).The absorbance (A) values of A549 cells transfected with miR-mimic were 0.451 ±0.051 and 0.518 ±0.074 on the third and forth day respectively,and those of A549 cells transfected with miR-NC were 0.683 ± 0.041 and 0.815 ± 0.065 respectively.The proliferation ability of miR-mimic group was significantly lower than that of miR-NC group (t =12.965,P ＜ 0.001;t =9.535,P ＜ 0.001).The colony forming rates of A549 cells transfected with miR-NC and miR-134 mimic were 91.2％ ± 8.3％ and 38.6％ ±4.5％ respectively,and the colony forming rate of A549 cells in miR-134 mimic group was significantly decreased (t =17.617,P ＜0.001).The apoptosis rates of miR-134 mimic group and miR-NC group were 93.5％ ± 3.7％ and 85.4％ ± 2.0％ respectively,and the difference was significant difference (t =6.119,P ＜ 0.001).The relative expressions of P53 protein in miR-134 mimic group and miR-NC group were 1.816 ±0.173 and 0.992 ± 0.096 respectively,and the difference was statistically significant (t =19.308,P ＜ 0.001).Conclusion miR-134 can be an effective target for the treatment of NSCLC by increasing the protein expression of P53,inhibiting the viability and proliferation of tumor cells,and promoting the apoptosis of tumor cells.

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-231:0.552 ± 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-231:0.472 ± 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.