南方医科大学学报

南方医科大学学报 ›› 2013, Vol. 33 ›› Issue (06): 812-.

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Id1/Id3在子宫内膜癌中的表达及对子宫内膜癌细胞生物学的作用

孙丽丽，李学农，刘国炳   

  • 出版日期:2013-06-20 发布日期:2013-06-20

Expression of Id1 and Id3 in endometrial carcinoma and their roles in regulating biological behaviors of endometrial carcinoma cells in vitro

  • Online:2013-06-20 Published:2013-06-20

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摘要： 目的探讨DNA分化抑制因子（inhibitor of DNA differentiation, Id）Id1/Id3在子宫内膜癌中的表达及对子宫内膜癌细胞
增殖、侵袭、迁移及粘附等生物学行为的作用。方法Western blot方法检测4例子宫内膜癌组织及相应的癌旁组织中的Id1/Id3
的表达；将子宫内膜癌RL-952和HEC-1-B两株细胞各分为未处理细胞组、空白病毒组、启动子病毒组和Id1/Id3双敲低组。通
过qRT-PCR检测不同腺病毒载体感染细胞后MMP2、CXCR4和P21 mRNA表达量，Western blot检测MMP2、CXCR4、P21蛋白
表达情况；通过MTT增殖试验、Transwell侵袭实验、细胞划痕实验和细胞粘附实验检测Id1/Id3表达改变后，对子宫内膜癌细胞
增殖、侵袭、移行和粘附能力的影响。结果Id1/Id3在子宫内膜癌组织中较癌旁组织表达增高（P<0.05）；双敲低Id1/Id3，子宫内
膜癌细胞中MMP2、CXCR4的mRNA水平和蛋白水平明显降低（P<0.05），P21的mRNA水平和蛋白水平则明显升高（P<0.05），
RNAi组与其他3组细胞相比均有显著性差异；Id1/Id3双敲低组子宫内膜癌RL-952和HEC-1-B株细胞增殖能力、侵袭能力、迁
移能力和粘附能力均抑制（P<0.05）。结论Id1/Id3在子宫内膜癌患者组织中高表达，并可通过升调MMP2、CXCR4和降调P21
的表达促进子宫内膜癌细胞增殖、侵袭、迁移及粘附作用，靶向Id1/Id3治疗可能成为预防和治疗子宫内膜癌的新方案。

Abstract: Objective To investigate the expression of inhibitor of DNA differentiation/DNA binding 1 (Id1) and Id3 in
endometrial carcinoma and explore their roles in regulating the proliferation, invasion, migration and adhesion of endometrial
carcinoma cells in vitro. Methods Id1 and Id3 expression in 4 fresh endometrial cancer tissue specimens and matched adjacent
tissues were detected using Western blotting. Two endometrial cancer cell lines, HEC-1-B and RL-952, were both divided into 4
groups, namely the untreated group, blank virus group, promoter group and Id1/Id3 double-knockdown group, and their
expressions of MMP2, CXCR4 and P21 were detected by qRT-PCR and Western blotting. The proliferation, invasion, migration
and adhesion of the cells were evaluated with MTT, Transwell, wound-healing, and adhesion assays. Results Endometrial
carcinoma tissues showed significantly higher Id1 and Id3 expression than the adjacent tissues (P<0.05). In the two endometrial
carcinoma cell lines, Id1/Id3 double-knockdown significantly decreased MMP2 and CXCR4 expression and increased P21
expression at both mRNA and protein levels (P<0.05), and resulted in suppressed cell proliferation, invasion, migration and
adhesion. Conclusions Id1 and Id3 expressions are up-regulated in endometrial carcinoma to promote the proliferation,
invasion, migration and adhesion of the tumor cells by increasing MMP2 and CXCR4 expression and reducing P21 expression.
Therapies targeting Id1/Id3 can be a novel strategy for treatment of endometrial carcinoma.