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作 者:王伟[1] 纪捷[1] 程雪[1] 张静敏[1] 郭凌川[2]
机构地区:[1]南京医科大学附属妇产医院病理科,南京210004 [2]苏州大学附属第一医院病理科,苏州215006
出 处:《临床与实验病理学杂志》2017年第11期1213-1218,共6页Chinese Journal of Clinical and Experimental Pathology
基 金:江苏省自然科学基金(BK20151078)
摘 要:目的探讨球状C1q受体(g C1qR)在卵巢癌中的表达,并分析其潜在的分子机制。方法收集48例卵巢癌组织和卵巢癌细胞株SKOV3为分析对象,采用PCR、Western blot分别检测g C1qR mRNA及蛋白质的表达;采用MTT比色法、Transwel实验及流式细胞技术检测卵巢癌细胞的增殖、迁移及凋亡情况;以分子荧光探针H2DCFDA、Fluo-3/AM、JC-1分别测定细胞内活性氧(ROS)、Ca^(2+)浓度以及线粒体膜电位,评估卵巢癌细胞线粒体功能的变化。结果卵巢癌组织中g C1qR mRNA及蛋白质表达分别为2.61±0.34、0.20±0.02,均明显低于其相应的癌旁正常卵巢组织7.32±1.25和0.67±0.06,差异有显著性(P<0.001)。g C1qR基因过表达,可显著降低卵巢癌细胞增殖活性、迁移率;其细胞凋亡率明显增加,且呈现显著的细胞凋亡特征;同时,卵巢癌细胞线粒体中ROS含量、细胞内Ca^(2+)浓度显著增高,线粒体膜电位显著减少。结论 g C1qR基因在卵巢癌细胞凋亡中发挥重要作用,可通过引发线粒体功能障碍诱导卵巢癌细胞凋亡。Purpose To investigate the expression of glob- ular C1 q receptor (gC1 qR) in ovarian cancer and to explore its potential molecular mechanism. Methods Retrospective analysis was made on 48 ovarian cancer tissues and ovarian cancer cell line SKOV3. Real time PCR and Western blot analysis were applied to detect the levels of gClqR mRNA and gClqR protein expression. The abilities of SKOV3 cells proliferation activity and quantity, migration and apoptosis were respectively assessed by MTT, transwell assay and flow cytometry. Besides, the intra- cellular ROS was estimated via the fluorescence of H2 DCFDA, the mitochondrial membrane potential was tested using a JC-1 probe, and the intracellular Ca2+ was assessed via Fluo-3/AM. Results The expressions of gClqR gene was obviously de- creased in the group of ovarian cancer tissues when compared with normal ovarian tissues group (2.61 ±0. 34 vs 7.32± 1.25, 0. 20 ± 0. 02 vs 0. 67 ± 0. 06, P 〈 0. 001 ). Overexpression of gClqR gene could result in significant up-regulation of ovarian cancer cell apoptosis and down-regulation in proliferation and migration, and showed significant cell apoptosis morphology. Simuhaneously, the intracellular ROS and Ca2+ were obviously increased, and the mitochondrial membrane potential was obvi- ously decreased. Conclusion gC1 qR gene may play an important role in the apoptosis of ovarian cancer cells. In this process, gClqR gene can induce apoptosis of ovarian cancer cells by inducing mitoehondrial dysfunction.
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