【摘要】 目的探讨miR-155对喉鳞癌Hep-2细胞增殖与侵袭的影响。方法应用LipofectamineTM2000将miR-155inhibitor和miR-155阴性对照(NC)转入Hep-2细胞,四甲基偶氮唑蓝(MTT)法检测细胞活力,Hoechst染色检测细胞凋亡情况,Transwell实验检测细胞侵袭能力,Western blot检测信号传导与转录激活因子3(STAT3)和细胞因子信号抑制因子1(SOCS1)的表达水平。结果与miR-155 NC组比较,miR-155 inhibitor能显著抑制肿瘤细胞增殖能力,提高肿瘤细胞凋亡率,降低细胞侵袭能力,并上调SOCS1,下调STAT3表达水平,差异均有统计学意义(P<0.05)。结论 miR-155可能通过SOCS1/STAT3信号通路促进Hep-2细胞增殖,抑制凋亡,并能提高细胞的侵袭能力,进而发挥致癌作用。更多还原

【Abstract】 Objective To investigate the effect of miR-155 on proliferation and invasion of laryngeal squamous cell carcinoma Hep-2 cells. Methods LipofectamineTM2000 was used to transfer miR-155 inhibitor and miR-155 negative control(NC) into Hep-2 cells. Cell viability was detected by MTT assay. Apoptosis was detected by Hoechst staining.Transwell assay was used to detect cell invasion ability. Signal transducers and activators of transcription 3(STAT3) and Suppressor of cytokine signaling 1(SOCS1) expression levels were detected by Western blot. Results Compared with miR-155 NC group, miR-155 inhibitor significantly inhibited the proliferation of tumor cells, increased the apoptosis rate of tumor cells, decreased the cell invasion ability, and up-regulated SOCS1 and down-regulated the expression of STAT3. The difference was statistically significant(P<0.05). Conclusion MiR-155 may promote the proliferation of Hep-2 cells, inhibit apoptosisand increase the invasive ability of cells through SOCS1/STAT3 signaling pathway, thereby promoting carcinogenesis.更多还原