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目的:探讨KDM5B对唾液腺腺样囊性癌侵袭、转移能力的调控作用。方法:通过q PCR验证唾液腺腺样囊性癌与正常组织中KDM5B的表达水平差异,以唾液腺腺样囊性癌肺转移细胞株SACC-83为实验对象,通过脂质体介导,将KDM5B-si R转染至SACC-83细胞,降低KDM5B的表达水平。采用荧光实时定量RT-PCR检测转染前、后SACC-83中KDM5B的表达变化,通过Transwell小室检测细胞侵袭、迁移能力的改变,Western印迹检测KDM5B的下游信号分子Akt的表达变化。应用SPSS 16.0软件包对所得数据进行t检验或单因素方差分析。结果:转染KDM5B-si R后的SACC-83中,KDM5B表达显著下调(P<0.01)。SACC-83细胞的侵袭、迁移能力显著降低(P<0.01)。Western印迹检测结果显示,在SACC-83细胞中降低KDM5B的表达水平后,Akt磷酸化水平升高,而Akt的表达水平不变。结论:高表达KDM5B有助于维持ACC的侵袭、转移特性,降低其表达水平则能有效抑制SACC-83的侵袭、迁移能力。KDM5B可能通过调控其下游信号通路基因Akt的磷酸化水平而发挥作用。
Objective: To investigate the role of KDM5B in the invasion and metastasis of salivary adenoid cystic carcinoma. Methods: The expression of KDM5B in salivary adenoid cystic carcinoma and normal tissues was verified by q PCR. SACC-83 cell line was used as the experimental group. The KDM5B- si R was transfected into SACC-83 cells to decrease the expression of KDM5B. The changes of KDM5B expression in SACC-83 cells before and after transfection were detected by real-time fluorescence quantitative RT-PCR. The changes of cell invasion and migration were detected by Transwell chamber. The expression of Akt in KDM5B was detected by Western blotting. The data obtained were t-test or one-way analysis of variance using SPSS 16.0 software package. Results: KDM5B expression was significantly down-regulated in SACC-83 cells transfected with KDM5B-si R (P <0.01). SACC-83 cell invasion, migration ability was significantly reduced (P <0.01). Western blot results showed that Akt phosphorylation was increased but Akt expression unchanged in SACC-83 cells after KDM5B was down-regulated. Conclusion: High expression of KDM5B can help maintain the invasion and metastasis of ACC and decrease the expression of KDM5B, which can effectively inhibit the invasion and migration of SACC-83. KDM5B may play a role in regulating the phosphorylation level of its downstream signaling pathway gene Akt.