【摘 要】
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Background: Human globular heads of C1q receptor (gC1qR) is a conserved eukaryotic protein that localizes predominantly in the mitochondrial matrix.The list of biologic response mediated by gClqR is i
【机 构】
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State key Laboratory of Reproductive Medicine, Department of Clinical Laboratory,Nanjing Maternity a
【出 处】
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2012年全国肿瘤分子标志学术大会与国际肿瘤转化医学论坛暨第七届中国中青年肿瘤专家论坛
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Background: Human globular heads of C1q receptor (gC1qR) is a conserved eukaryotic protein that localizes predominantly in the mitochondrial matrix.The list of biologic response mediated by gClqR is indeed extensive, which include important functions that play major roles in phagocytosis and the uptake of apoptotic cells.The purpose of this study was to investigate the effect of p53 on the apoptosis of gClqR-induced human cervical cancer cell line (C33a).Methods: Here human cervical tissues were examined for the expression of gClqR using Real-time PCR and Western blot analysis.Apoptotic death of C33a cells was assessed by flow cytometric analysis to detect the subG1 population.Viability,migration and proliferation of C33a cells were detected via water-soluble tetrazolium salt (WST-1) assay, Transwell assay, 3H-thymidine incorporated into DNA assay (3H-TdR)respectively.Results: Here we showed that the gClqR protein was significantly down-regulated expression in human cervical cancer tissue.Cells transfected with a GFP-gClqR vector resulted in up-regulated gC1qR protein and a gradual increase in the generation of reactive oxygen species (ROS).Additionally, ROS generation and increased Ca2+ influx in mitochondria resulted in the loss of the mitochondrial transmembrane potential.Meanwhile, over-expression of gC1qR can induce the p53 expression and the C33a apoptosis.When gC1qR was overexpressed in C33a cells, the change of mitochondrial function was abrogated by a trans-dominant negative mutant of p53, Further, upon overexpression of gC1qR, cell viability, migration and proliferation were shown to be significantly enhanced when cells were treated with mutant p53.Conclusion: These data indicate that gC1qR plays an important role in cervical cancer cell apoptosis, moreover, gC1qR-induced C33a apoptosis is p53-dependent.
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