CAJ | 학술논문

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。
목적：연구 MALAT1대방광암 UMUC3세포계증식、천이、침습、극륭형성능력적영향，탐토MALAT1재방광암중적작용궤제。방법화학합성침대 MALAT1적 siRNA ，지질체법전염UMUC3세포。반전록실시정량취합매련식반응（RT-qPCR）측정전염효솔，MTS 법검측증식변화，Transwell 법검측천이、침습개변，극륭형성실험관찰극륭형성능력변화，5-을결기-2′-탈양뇨감（EDU）법검측증식급주기개변，기인심편사선잠재작용통로。결과간우 MALAT1표체후，방광암 UMUC3세포주증식、침습、천이、극륭형성능력하강，기인심편결과발현종류통로상관기인 MMP9등명현개변。결론 MALAT1촉진 UMUC3방광암세포적증식、침습、천이、극륭형성능력，제시가능여기인기종류통로상관기인적격활화실활상관。
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.