目的 研究MALAT1对膀胱癌UMUC3细胞系增殖、迁移、侵袭、克隆形成能力的影响,探讨MALAT1在膀胱癌中的作用机制。方法 化学合成针对MALAT1的siRNA,脂质体法转染UMUC3细胞。反转录实时定量聚合酶链式反应(RT-qPCR)测定转染效率,MTS法检测增殖变化,Transwell法检测迁移、侵袭改变,克隆形成实验观察克隆形成能力变化,5-乙炔基-2′-脱氧尿苷(EDU)法检测增殖及周期改变,基因芯片筛选潜在作用通路。结果 干扰MALAT1表达后,膀胱癌UMUC3细胞株增殖、侵袭、迁移、克隆形成能力下降,基因芯片结果发现肿瘤通路相关基因MMP9等明显改变。 结论 MALAT1促进UMUC3膀胱癌细胞的增殖、侵袭、迁移、克隆形成能力,提示可能与其引起肿瘤通路相关基因的激活和失活相关。
Objective To investigatethe effect of MALAT1 on regulationof proliferation, migration, invasion, clone formation, and other functions in UMUC3 cell lines of bladder cancer, and to explore the molecular mechanism of MALAT1 in bladder cancer. Methods Thesmall interfering RNA (siRNA) was designed and synthesized and then transfected into the UMUC3 cells. The transfection efficiency was detected with RT-QPCR assay. MTS assay, transwell migration and matrigel invasion assay, colony formation assay and 5-ethinyl-2′-deoxyuridine (EDU) assay were performed to evaluate the proliferation, migration, invasion, clone formation and cell cycle respectively. To explore the potential pathways of MALAT1, we performed gene chip assay. Results After down regulation the expression of MALAT1, the proliferation, invasion, migration and colony-forming ability of UMUC3 bladder cancer cells were impaired. Gene chip found that cancer pathways related gene changed obviously after knockdown of MALAT1 in UMUC3 cells. Conclusion MALAT1 promoted the proliferation, invasion, migration, cell cycle and clone formation ability in UMUC3 cell lines of bladder cancer through modulating the cancer pathways related gene activation and deactivation.