论文部分内容阅读
[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CalphostinC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CalphostinC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CalphostinC可明显抑制L9981肺癌细胞株的细胞增殖力和侵袭力;CalphostinC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。
[Objective] To explore the feasibility of using PKC as a target to develop anti-tumor invasion and metastasis-targeting drugs using its specific inhibitor. [Method] The invasion and proliferation of three lung cancer cell lines (L9981, L9981-pLXSN and L9981-nm23-H1) were detected by MTT assay and modified Boyden chamber assay respectively. After addition of CalphostinC, Invasion, Proliferation changes. [Results] The invasiveness and proliferation activity of L9981 and L9981-pLXSN in vitro were significantly higher than those in L9981-nm23-H1 lung cancer cell line transfected with nm23-H1 (P <0.001). The in vitro invasiveness and proliferation of L9981 and L9981- Activity was no significant difference (P> 0.05). However, the invasive and proliferative activity of L9981-nm23-H1 cells in vitro was still lower than that of L9981 and L9981-pLXSN cells (P <0.001) ), But there was no significant difference between the two cells (P> 0.05). [Conclusion] The PKC inhibitor Calphostin C can significantly inhibit the cell proliferation and invasiveness of L9981 lung cancer cell lines. Calphostin C and nm23-H1 have synergistic and invasive effects on the proliferation and invasiveness of human high metastatic large cell lung cancer cell lines in vitro Additive effect.