Rap1酶激动剂C3G对Ⅰ型卵巢癌细胞增殖和侵袭的影响

李雪梅; 罗淑娟; 车亚玲; 令狐华

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Rap1酶激动剂C3G对Ⅰ型卵巢癌细胞增殖和侵袭的影响

论著 | 更新时间：2026-01-09

- Rap1酶激动剂C3G对Ⅰ型卵巢癌细胞增殖和侵袭的影响
- Effect of Rap1 activator C3G on proliferation and invasion in type Ⅰ ovarian cancer cells
- 陆军军医大学学报 2015年37卷第17期页码：1715-1719
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  中图分类号： R394.3;R730.23;R737.31
- 纸质出版：2015
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李雪梅,罗淑娟,车亚玲,令狐华.Rap1酶激动剂C3G对Ⅰ型卵巢癌细胞增殖和侵袭的影响[J].陆军军医大学学报(原第三军医大学学报),2015,37(17):1715-1719.

　Li Xuemei,Luo Shujuan,Che Yaling,Linghu Hua.Effect of Rap1 activator C3G on proliferation and invasion in type Ⅰ ovarian cancer cells[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(17):1715-1719.
李雪梅,罗淑娟,车亚玲,令狐华.Rap1酶激动剂C3G对Ⅰ型卵巢癌细胞增殖和侵袭的影响[J].陆军军医大学学报(原第三军医大学学报),2015,37(17):1715-1719. DOI：

　Li Xuemei,Luo Shujuan,Che Yaling,Linghu Hua.Effect of Rap1 activator C3G on proliferation and invasion in type Ⅰ ovarian cancer cells[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(17):1715-1719. DOI：

摘要

目的探讨Rap1酶激动剂鸟苷酸交换因子（Crk SH3-domain-binding guanine nucleotide-releasing factor，C3G）对Ⅰ型卵巢癌恶性增殖及侵袭能力的影响。方法 Western blot分别检测Ⅰ型和Ⅱ型人卵巢癌组织中C3G蛋白的表达水平；利用Ⅰ型卵巢癌细胞株OVAR3，构建外源性过表达C3G蛋白的细胞株，通过MTT、平板克隆、流式细胞学实验检测细胞的增殖和凋亡情况；Transwell检测细胞迁移、侵袭能力；Western blot检测细胞MMP-2、MMP-9的表达。结果 Ⅰ型卵巢癌组织中C3G表达（0.377 6±0.083 1）与良性卵巢肿瘤（0.351 1±0.071 3）及正常对照类似，明显低于Ⅱ型卵巢癌组织[（0.873 5±0.174 6)，P0.05]。低转移潜能卵巢癌细胞株OVAR3在外源表达C3G后表现出增殖减慢（P0.05

P0.01），凋亡增加（P0.05），但迁移和侵袭能力增强（P0.05），MMP-2、MMP-9表达增高（P0.05）。结论 C3G蛋白有抑制增殖和促进侵袭作用，其在Ⅰ型卵巢癌组织中的低表达与其低转移潜能和膨胀型生长模式相关。

Abstract

Objective To investigate the effect of guanine nucleotide exchange factor Crk SH3-domain-binding guanine nucleotide-releasing factor (C3G) on malignant proliferation and invasion of type Ⅰ ovarian cancer. Methods C3G expression in 6 samples of type Ⅰ and 43 samples of Ⅱ ovarian cancer tissues was detected by Western blotting. Exogenous C3G was transferred into type Ⅰ ovarian cancer cell line OVCAR3

and MTT assay

plate clone assay and flow cytometry were performed to analyze cell proliferation and apoptosis. Transwell chamber assay was adopted to evaluate cell invasion and migration. MMP-2 and MMP-9 expressions were examined by Western blotting. Results C3G expression in type Ⅰ ovarian cancer tissues (0.377 6±0.083 1) was similar to that in benign tumor tissues (0.351 1±0.071 3) and normal controls (0.336 2±0.073 9)

but was lower than that in type Ⅱ ovarian cancer tissues (0.873 5±0.174 6

P0.05). After C3G was over-expressed in the OVAR3 cells

cell proliferation was inhibited (P0.05)

and cell apoptosis was increased (P0.05). Meanwhile the migration and invasion capacity was enhanced (P0.05)

and the expression of MMP-2 and MMP-9 was up-regulated (P0.05). Conclusion C3G can inhibit proliferation and promote invasion in OVCAR3 cells

and its low expression in type Ⅰ ovarian cancer is associated with swelling growth and low metastatic potential.

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