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高转移人肺巨细胞癌ＰＧ细胞恶性表型明显。以人胚肺细胞为对照，荧光染料标记示踪法表明，ＰＧ的间隙连接通讯功能缺陷；免疫荧光染色显示微管解聚；荧光鬼笔环肽染色显示微丝网架破坏。分子杂交结果表明，ＰＧ细胞有ｃ－ｍｙｃＤＮＡ扩增和ｃ－Ｈａ－ｒａｓ、ｃ－ｍｙｃ基因高表达，抑癌基因Ｐ５３ｍＲＮＡ水平低于正常。用钙调蛋白拮抗剂ＣＤＺ（１００～２００ｎｍｏｌ／Ｌ）和中药Ｌ２（３～１３ｍｇ／ｍｌ）分别处理ＰＧ，细胞增殖受到抑制，表型向正常分化，细胞通讯功能再现，微管网架恢复。但只有Ｌ２能促进微丝骨架恢复，抑制软琼脂内的集落形成，并使ｃ－ｍｙｃ扩增减弱和ｍＲＮＡ水平下降，Ｐ５３表达升高。
Highly metastatic human lung giant cell carcinoma PG cells have a prominent malignant phenotype. Using human embryonic lung cells as a control, the fluorescent dye-labeled tracer method showed that gap junctional communication function defects of PG; immunofluorescence staining showed microtubule depolymerization; and fluorescent phalloidin staining showed disruption of the microfilament frame. The results of molecular hybridization indicated that c-mycDNA and c-Ha-ras and c-myc genes were highly expressed in PG cells, and the P53 mRNA level of tumor suppressor gene was lower than normal. PG was treated with the calmodulin antagonist CDZ (100-200 nmol/L) and the traditional Chinese medicine L2 (3-13 mg/ml), and cell proliferation was inhibited. The phenotypes were normalized, cell communication function was reproduced, and the microtubule network was restored. However, only L2 can promote the recovery of microfilament skeleton, inhibit the colony formation in soft agar, weaken the c-myc amplification and decrease the mRNA level, and increase the expression of P53.