ABSTRACT
Objective To investigate the mechanism of Mi-362 targeting Six1 inhibiting proliferation and migration of cer-vical cancer cells. Methods The expression levels of microRNA-362 in cervical cancer tissues and adjacent tissues were measured in 142 patients with cervical cancer in our hospital. At the same time,Hela cancer cell group,microRNA-362 mimics group and mi-croRNA-362 inhibitor group were set up to determine the viability of cancer cells,the number of monoclonal formation of cancer cells,the apoptotic rate of cancer cells,cell cycle,the number of perforations,and the levels of microRNA-362 and Six1 in cervical cancer fluid of Hela. Results The expression level of miR-362 in cervical cancer tissue was lower than that in adjacent tissue(P<0. 05). The higher the infiltration of lymphatic vessel space,pathological stage,TNM stage,lymph node metastasis and depth of infil-tration,the lower the expression rate of miR-362(P<0. 05). The OD value and survival rate in the miR-362 mimics group were lower than those in the Hela cancer cells group(P<0. 05),while the OD value and survival rate in the mir-362 inhibitor group were higher than those in the Hela cancer cells group and the miR-362 mimics group(P<0. 05). The number of clones formed in the miR-362 mimics group was lower than that in the Hela cancer cell group(P<0. 05),and the number of clones formed in the miR-362 inhibitor group was higher than that in the Hela cancer cell group and the miR-362 mimimics group(P<0. 05). The apoptotic rate of miR-362 mimics group was higher than that of Hela cancer cell group(P<0. 05),and that of miR-362 inhibitor group was lower than that of Hela cancer cell group and miR-362 mimics group(P<0. 05). The G1 phase in the miR-362 mimics group was higher than that in the Hela cancer cell group(P<0. 05),and the G1 phase in the miR-362 inhibitor group was lower than that in the Hela cancer cell group and the miR-362 mimimics group(P<0. 05). The number of cell membrane penetration in the miR-362 mimics group was lower than that in the Hela cancer group(P < 0. 05),and that in the miR-362 inhibitor group was higher than that in the Hela cancer group and the miR-362 mimimics group(P<0. 05). The expression level of miR-362 in the miR-362 mimics group was higher than that in the Hela cancer cell group(P<0. 05),and the expression level of miR-362 in the miR-362 inhibitor group was lower than that in the Hela cancer cell group and the miR-362 mimics group(P<0. 05). The expression level of Six1 in the miR-362 mimics group was lower than that in the Hela cancer cell group(P<0. 05),and that in the miR-362 inhibitor group was higher than that in the Hela cancer cell group and the miR-362 mimics group(P<0. 05). Conclusion miR-362 plays an important inhibition in the occurrence and development of cervical cancer,and its mechanism is related to the inhibition of prolifer-ation,migration and invasion of cancer cells by microRNA-362 through negative regulation of Six1.
ABSTRACT
Objective To detect the expression of human epithelial growth factor receptor 2 (HER-2) in advanced lung adenocarcinoma with epithelial growth factor receptor (EGFR) mutation, and to explore the potential of HER-2 as a therapeutic target for drug resistance in patients with EGFR mutations. Methods HER-2 is commonly expressed in the advanced lung adenocarcinoma with EGFR mutations, mainly in the cell membrane. Results The overexpression rate of HER-2 protein in tissues of advanced lung adenocarcinoma with EGFR mutations was 33.3%(28/84). The overexpression rate of HER-2 protein in patients>50 years of age was 40.3%(27/67), which was significantly higher than that of patients ≤50 years of age [5.9 % (1/17)], the difference was statistically significant (χ2=7.227, P=0.007). The overexpression rate of HER-2 protein in patients with high pathological differentiation [44.4 % (8/18)] was higher than that in patients with poor pathological differentiation [30.3%(20/66)], but the difference was not statistically significant (χ2=1.273, P=0.259). The overexpression of HER-2 protein in patients with EGFR 21 exon mutation [40.5 % (17/42)] was significantly higher than that of EGFR19 exon mutation [25.0%(10/40)], but the difference was not statistical significance (χ2=2.222, P=0.136). Conclusions The overexpression rate of HER-2 protein in advanced lung adenocarcinoma patients with EGFR mutation is high, which is related to the age and tumor differentiation. HER-2 is expected to be a potential therapeutic target for drug resistance patients with EGFR mutations.