机构地区:[1]上海交通大学附属仁济医院妇产科,上海200001
出 处:《中国癌症杂志》2006年第11期911-914,共4页China Oncology
基 金:2004年国家自然科学基金资助项目(编号:30471808)。
摘 要:背景与目的:HIF-1α是一个在缺氧状态下重要的转录调节因子,控制调节各种由缺氧引起的相关基因表达,参与肿瘤的恶化、浸润和转移,在肿瘤领域已成为研究热点。本文主要研究CoCl2模拟化学缺氧复氧中HIF-1α的表达,及其对人卵巢癌HO-8910PM细胞株生物学行为的影响。方法:在培养基中加入和去除CoCl2模拟化学缺氧和缺氧复氧,采用逆转录-聚合酶链反应(RT-PCR)检测CoCl2与HIF-1α的mRNA转录的量-效和时-效关系;通过MTT、Boyden小室、细胞黏附试验分别检测细胞生长、侵袭力和黏附力。结果:人卵巢癌HO-8910PM细胞株中存在HIF-1α的mRNA转录;在CoCl2模拟缺氧的时-效关系实验中,150μmol/LCoCl2刺激细胞8h、16h、24h时HIF-1αmRNA转录呈递增(分别为2.11±0.03、2.52±0.05、2.78±0.11)(P<0.05),24h达高峰,48h明显下降。同时,在量-效关系实验中,100μmol/L、150μmol/L刺激细胞16h时HIF-1αmRNA转录呈递增(分别为1.54±0.03、2.07±0.13)(P<0.05);MTT发现CoCl2诱导的缺氧对细胞生长起抑制作用;Boyden小室检测细胞侵袭力实验发现缺氧16h复氧24h后细胞的侵袭力增加(穿越细胞膜的细胞数86±9,较对照组53±10增加)(P<0.05);细胞黏附实验发现缺氧16h复氧24h后细胞的黏附力增加(P>0.05)。结论:CoCl2能诱导HO8910-PM细胞HIF-1α的过度转录,而且存在一定的时-效关系;经缺氧后复氧,肿瘤细胞的侵袭力和黏附力增加,且肿瘤细胞的侵袭力增加统计学差异显著。Background and purpose: HIF-1α (Hypoxia-inducible factor-1α) is an important transcription factor under hypoxia condition. It plays the role of dominating the expressions of correlative genes. It also promotes tumor deterioration, tumor metastasis and tumor invasion. The molecular role of HIF-1α has been intensively studied in cancer basic research. This article is to investigate the expression of HIF-1α under hypoxic and reoxygenation induced by CoCl2 and the impact of hypoxia-inducible transcription factor-1α on human ovarian carcinoma cell line HO-8910PM. Methods: Semi quantitative reverse transcription-polymerase chain reaction (RT-PCR) is performed to detect the expression of HIF-1α mRNA in human ovarian carcinoma cell HO-8910PM exposed during the phase of hypoxia and reoxygenation. The relations of the quantity-efficiency and the time-efficiency were analyzed. The effects of HIF-1α gene on the proliferation, invasion and adhesion of HO-8910PM cell were estimated by either MTT, Boyden cell or cell adhesion tests. Results: There was endogenous expression of HIF-1α in human ovarian carcinoma cell line HO-8910PM. RT-PCR show that over-expression of HIF-1α mRNA could be measured under hypoxia induced by CoCl2(P 〈0.05). The expression of HIF-1α was in quantity- and time-dependent manner under a hypoxic situation. The fastigum was at 24 hours after ceils stimulated by CoCl2. The hypoxia induced by CoCl2 had a prohibitive.effect on cell proliferation evaluated by MTT. After hypoxia for 16 hours and reoxygenation for 24 hours, the invasive and adhesive abilities of cell have been enhanced. Conclusions: CoCl2 could induce the over-expression of HIF-1α in human ovarian carcinoma cell line HO-8910PM. And there is time-dependent response under some circumstances . The invasive and adhesive abilities of cell can be augmented under chemical hypoxia and reoxygenation.
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