论文部分内容阅读
目的探讨ＮＭ２３／ＮＤＰＫ在癌细胞转移行为涉及的跨膜信息传递中的作用。方法选用具不同转移潜能的小鼠前胃癌克隆细胞株（ＭＦＣ），用ＵＴＰ生成及乳酸脱氢酶－丙酮酸脱氢酶激酶偶联法、受体放射性竞争结合法和Ｂｏｙｄｅｎ小室法分别对其ＮＤＰＫ活性、ＩＰ３含量、侵袭力及ＬＮ和ＥＧＦ对上述指标的影响进行了测定。结果与高转移细胞相比，转移性较低的细胞的ＮＤＰＫ活性较强。ＩＰ３含量较高，侵袭能力较弱，对ＥＧＦ的反应较强，但两者对ＬＮ的反应无明显差别。结论ＮＤＰＫ具有调节ＭＦＣ转移的作用。推测其调节机制可能是影响Ｇ蛋白的效应，且对胞外信息有选择性。
Objective To investigate the role of NM23 / NDPK in the transmission of transmembrane information involved in cancer metastasis. Methods Mouse gastric precancerous cell clonal cell line (MFC) with different metastatic potentials was selected. UTP production and lactate dehydrogenase - pyruvate dehydrogenase kinase coupling method, receptor radio competition binding method and Boyden chamber method were used respectively NDPK activity, IP3 content, invasiveness and the effects of LN and EGF on the above indexes were measured. Results Compared with highly metastatic cells, cells with lower metastasis showed stronger NDPK activity. IP3 content is higher, invasion ability is weaker, the response to EGF is stronger, but there is no significant difference between them. Conclusion NDPK has the function of regulating MFC metastasis. It is speculated that the regulatory mechanism may affect the effect of G protein, and selective extracellular information.