【作者】 马力；

【导师】 周清华；

【作者基本信息】 四川大学 ， 肿瘤学， 2006， 博士

【摘要】 研究背景与目的：肺癌的侵袭和转移是肺癌的恶性标志和特征，也是导致肺癌患者治疗失败和死亡的主要原因。肺癌的侵袭和转移是一个多因素作用、多基因参与、涉及细胞多个信号通路改变，并经过多个阶段才最终形成的复杂生物过程。因此，探讨肺癌侵袭转移相关细胞信号传导通路的变化，不仅有助于揭示肺癌侵袭转移的分子机制，而且将为阻断肺癌侵袭转移的信号传导和逆转肺癌侵袭转移表型提供新的靶点和途径。我们的前期研究工作已经证明肿瘤转移抑制基因nm23-H₁的低表达、杂合性缺失和突变与肺癌的高转移性和预后不良有密切关系，并在调控“肺癌转移抑制级联”中发挥上游关键基因的作用。人高转移大细胞肺癌细胞株L9981中转染野生型nm23-H₁基因后，nm23-H₁可通过调控“肺癌转移抑制级联”中多个转移相关基因的表达，逆转肺癌细胞的转移表型。nm23-H₁基因对“肺癌转移抑制级联”的调控作用可能是通过细胞更多还原

【Abstract】 Background and objectives: Tumor metastasis is not only the malignant marker and characteristics of lung cancer, but also the main cause of failure to cure and lose their life of the patients with lung cancer. It is a complex biological behavior that associated with many factors, genes, signal pathways and processes. Therefore, to explore the changes of cell signal transduction related to invasion and metastasis in lung cancer will not only illuminate the molecular mechanism of tumor invasion and metastasis, but also provide a new targeting molecule and route for blocking signal transduction and reversing metastatic phenotype of lung cancer. Our previous researching works have proved that low expression and hetero-deletion of tumor metastasis suppressor gene nm23-H₁ was closely correlated with the high metastasis ability and poor prognosis of patient with lung cancer. nm23-H₁ gene is a key and更多还原