LncRNA －MALAT1在缺氧诱导胃癌侵袭转移中的作用

摘要

Objective:To explore the effect of LncRNA -MALAT1 on metastasis and invasion in gastric cancer cell SGC7901 and MKN45 under normoxia and hypoxia conditions.Methods:Using Real -time PCR to detect the ex-pression of MALAT1 in gastric cancer tissue and cell lines.Employing the small interfering RNA(siRNA)technique to observe the effect of knockdown of MALAT1 on human gastric cancer cell metastasis and invasion in vitro.Results:MALAT1 was highly expressed in gastric cancer tissues and cell lines compared with adjacent gastric tissues and gas-tric epithelial mucosa cells.Hypoxia significantly increased the migration and invasion potential of SGC7901 and MKN45,which was consistent with previous reports.After transfection with an siRNA to decrease endogenous MAL-AT1 expression,the hypoxia -induced migration and invasion of SGC7901 and MKN45 cells were dramatically dimin-ished.Conclusion:LncRNA -MALAT1 expression is increased in hypoxic GC and promotes hypoxia -induced GC metastasis and invasion.MALAT1 maybe an important target for therapy of metastasis in gastric cancer.%目的：探讨 LncRNA －MALAT1对缺氧诱导胃癌侵袭转移的影响。方法：RT －PCR 检测胃癌组织标本和胃癌细胞株中 MALAT1的表达；通过基因重组方法构建 MALAT1的 siRNA 载体，并感染人 SGC7901及MKN45胃癌细胞，RT －PCR 验证 siRNA 干扰有效；Transwell 实验研究其对胃癌细胞 SGC7901及 MKN45侵袭转移能力的影响。结果：MALAT1在胃癌组织和胃癌细胞株中的表达高于癌旁组织和胃正常上皮细胞；缺氧能够促进 SGC7901及 MKN45细胞的侵袭转移能力，而下调 MALAT1能够明显抑制缺氧条件下 SGC7901及MKN45细胞的侵袭转移能力。结论：MALAT1在促进胃癌细胞的侵袭转移中发挥重要作用，为胃癌靶向治疗提供理论依据。