[目的]探讨以蛋白激酶C(PKC)为靶点应用其特异性抑制剂开发抗肿瘤侵袭与转移靶向药物的可行性。[方法]应用MTT法和改良Boyden小室法分别检测三株肺癌细胞株细胞(L9981、L9981-pLXSN和L9981-nm23-H1)的侵袭力、增殖力;以及加入Calphostin C作用后,三株细胞株细胞侵袭力、增殖力的变化。[结果]L9981和L9981-pLXSN体外侵袭力和增殖活性明显高于转染nm23-H1基因的L9981-nm23-H1肺癌细胞株(P〈0.001);L9981和L9981-pLXSN细胞间体外侵袭力和增殖活性则无显著性差异(P〉0.05)。用Calphostin C处理三株肺癌细胞株后,细胞体外侵袭力和增殖活性显著下降(P〈0.001),但L9981-nm23-H1细胞体外侵袭力和增殖活性仍低于L9981和L9981-pLXSN(P〈0.001),而后两者细胞间则无显著性差异(P〉0.05)。[结论]PKC抑制剂Calphostin C可明显抑制L9981肺癌细胞株的细胞增殖力和侵袭力;Calphostin C和nm23-H1在影响人高转移大细胞肺癌细胞株细胞体外增殖活性和侵袭力的过程中具有协同和相加作用。
[Purpose ] To explore the possibility to develop anti-invasive and anti-metastatic targeted drug with protein kinase C (PKC) inhibitor. [Methods] Invasion and proliferation effect among different human pulmonary carcinoma cells (L9981, L9981-pLXSN and L9981-nm23-H1) were detected by Boyden Chamber Moder and MTT method, meanwhile these three lung cancer cell lines were treated with PKC inhibitor Calphostin C, and the same detection was performed. [Results] The invasion and proliferation ability in vitro of L9981 and L9981-pLXSN was higher than that of L9981-nm23-Hi lung cancer cell line which was transfected with nm23-H1 gene (P〈0.001). There was no difference beteween L9981 and L9981-pLXSN cell lines (P〉0.05). After treated with PKC inhibitor Calphstin C,the invasion and proliferation ability of three lung cancer cell lines were obviously descent(P〈0.001 ). However, the invasion and proliferation ability of L9981-nm23-H1 cell line was still weaker than those of L9981 and L9981-pLXSN lung cancer cell lines(P〈0.001 ); and there was also no difference between the latter two cell lines(P〉0.05 ). [Conclusions ] PKC inhibitor Calphostin C can downregulate the cell proliferation and invasion ability in L9981 lung cancer line. The effect of Calphostin C and nm23-H1 Knight be synergetic and added on invasion and proliferation ability in vitro of human high-metastatic large cell lung cancer cells.