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[摘要]
目的 探讨地榆皂苷I对卵巢癌细胞增殖、侵袭和迁移的影响及分子机制。方法 人卵巢癌A2780细胞分别用7.5、15.0、30.0 μmol/L的地榆皂苷I处理,同时设置si-NC组、si-IGFL2-AS1组、地榆皂苷I+pcDNA-IGFL2-AS1组、地榆皂苷I+pcDNA组;MTT检测细胞增殖抑制率;克隆形成实验检测细胞克隆形成数;Transwell法检测迁移和侵袭细胞数;Western blotting法检测E-钙黏蛋白(E-cadherin)和N-钙黏蛋白(N-cadherin)表达;双荧光素酶报告实验检测IGFL2-AS1和miR-138-5p的靶向关系。结果 不同浓度的地榆皂苷I处理A2780细胞后,细胞增殖、迁移和侵袭能力显著减弱(P<0.05),E-cadherin和miR-138-5p表达上调(P<0.05),N-cadherin和IGFL2-AS1表达下调(P<0.05),呈剂量相关性。下调IGFL2-AS1抑制A2780增殖、迁移及侵袭(P<0.05)。IGFL2-AS1靶向调控miR-138-5p,过表达IGFL2-AS1可减弱地榆皂苷I对A2780细胞增殖、迁移和侵袭的作用(P<0.05)。结论 地榆皂苷I通过调控IGFL2-AS1/miR-138-5p抑制卵巢癌细胞增殖、侵袭和迁移。
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[Abstract]
Objective To explore the effect and molecular mechanism of ziyuglycoside I on proliferation, invasion and migration of ovarian cancer cells. Methods Ovarian cancer cells A2780 were treated with 7.5, 15.0, 30.0 μmol/L of ziyuglycoside I. At the same time, si-NC group, si-IGFL2-AS1 group, ziyuglycoside I + pcDNA-IGFL2-AS1 group and ziyuglycoside I + pcDNA group were set up. MTT was used to detect proliferation inhibition rate of cells; Clone formation experiment was used to detect cell clone formation number; Transwell method was used to detect the numbers of migrating and invading cells; Western blotting was used to detect E-cadherin and N-cadherin protein expressions; Dual luciferase reporter experiment was used to detect the targeting relationship between IGFL2-AS1 and miR-138-5p. Results After treatment of A2780 cells with different concentrations of ziyuglycoside I, cell proliferation, migration and invasion were significantly weakened (P < 0.05), expressions of E-cadherin and miR-138-5p were up-regulated (P < 0.05), and the expressions of N-cadherin and IGFL2-AS1 were down-regulated in a dose-dependent manner (P < 0.05). After down-regulating IGFL2-AS1, the proliferation, migration and invasion of A2780 cells were inhibited (P < 0.05). IGFL2-AS1 targeted and regulated miR-138-5p. Overexpression of IGFL2-AS1 could attenuate the effects of ziyuglycoside I on proliferation, migration and invasion of A2780 cells (P < 0.05). Conclusion Ziyuglycoside I inhibits the proliferation, invasion and migration of ovarian cancer cells by regulating IGFL2-AS1/miR-138-5p.
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