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目的：研究卵巢癌细胞的浸润性。方法：采用膜浸润培养系统（ＭｅｍｂｒａｎｅＩｎｖａ－ｓｉｏｎＣｕｌｔｕｒｅＳｙｓｔｅｍ．ＭＩＣＳ）及重建基底膜模式（ＲｅｃｏｎｓｔｒｕｃｔｉｏｎｏｆＢａｓｅｍｅｎｔＭｅｍｂｒａｎｅ）定量研究卵巢癌细胞的浸润性。用细胞外介质胶（ｍｅｔｒｉｇｅｌ）涂布微孔碳素膜构成重建基底膜形成酷似活体中癌细胞所处的环境，以真实定量地反映癌细胞的浸润力。结果：用以试验的６种卵巢癌细胞株Ｂｉｘｌｅｒ、Ｂｉｘ３、Ｂｉｘ２ＮＭＢ．Ｈｅｙ、ＤＫ２ＮＭＡ及ＳＫＯＶ－３浸润基底膜的能力不同，Ｂｉｘｌｅｒ浸润能力最强，为１０．４４％。Ｈｅｙ次之，为８％，Ｂｉｘ３最弱。仅为０．６３±０．０８％。卵巢癌细胞株的浸润性与尿激酶类纤溶激活因子（ｕＰＡ）的基因转录表达有关，与克隆刺激因子（ＣＳＦ－１）的基因转录表达高度相关，ｒ＝０．Ｐ＜０．０１。以外源性ＣＳＦ－１处理癌细胞。则ｕＰＡＲＮＡ转录及该细胞的浸润性均增加２倍，说明卵巢癌细胞的浸润性受ｕＰＡ介导及ＣＳＦ－１调控。外源性ｕＰＡ抗体处理使卵巢癌细胞株的浸润能力阻断５０％。结论：卵巢癌细胞具有分泌ｕＰＡ的能力，是其具有浸润性的重要机制，但不是全部机制。关键词
Objective: To study the invasiveness of ovarian cancer cells. Methods: The invasiveness of ovarian cancer cells was quantified by Membrane Invasion Culture System (MICS) and Reconstruction of Basement Membrane (MEM). Microporous carbon membranes are coated with extracellular matrix (metrigel) to form a reconstructed basement membrane that resembles the environment in which live cancer cells are located to truly and quantitatively reflect the invasiveness of cancer cells. RESULTS: Six ovarian cancer cell lines, Bixler, Bix3, Bix2NMB, were tested. Hey, DK2NMA and SKOV-3 infiltrated the basement membrane of different ability, Bixler infiltration ability strongest, 10.44%. Hey followed by 8%, Bix3 the weakest. Only 0.63 ± 0.08%. The invasiveness of ovarian cancer cell lines was related to the transcriptional expression of urokinase-type plasminogen activator (uPA), which was highly correlated with the gene transcription and expression of CSF-1 (r = 0). P <0.01. Exogenous CSF-1 treated cancer cells. UPARNA transcription and cell infiltration were increased by 2 times, indicating that the invasiveness of ovarian cancer cells by uPA-mediated and CSF-1 regulation. Exogenous uPA antibody treatment blocked the invasive ability of ovarian cancer cell lines by 50%. Conclusion: Ovarian cancer cells have the ability of secreting uPA, which is an important mechanism of its infiltration, but not the whole mechanism. Key words