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为了探讨蛋白激酶Ｃα（ＰＫＣα）及其与环腺苷酸－蛋白激酶Ａ（ｃＡＭＰ－ＰＫＡ）信号系统的相关性，用六甲撑双乙酰胺（ｈｅｘａｍｅｔｈｙｌｅｎｅｂｉｓａｃｅｔａｍｉｄｅ，ＨＭＢＡ）和ＰＫＣ抑制剂ＣａｌｐｈｏｓｔｉｎＣ分别处理人肺癌细胞ＬＴＥＰａ－２，统计细胞生长百分数，测定ｃＡＭＰ水平。用斑点杂交方法检测ＰＫＣα基因表达，并测定表达反义ＰＫＣα的人肺癌ＬＴＥＰａ－２细胞中ＰＫＣ与ＰＫＡ激酶活性。结果显示：５μｍｏｌ／ＬＨＭＢＡ处理人肺癌ＬＴＥＰａ－２细胞３ｄ后，细胞增殖明显被阻抑，ＰＫＣα基因表达下降，ｃＡＭＰ水平升高。０．１５ｍｇ／ＬＰＫＣ抑制剂ＣａｌｐｈｏｓｔｉｎＣ导致人肺癌细胞增殖速度减慢时，ｃＡＭＰ水平也升高。在表达反义ＰＫＣα的人肺癌ＬＴＥＰα－２细胞中，当ＰＫＣα基因和蛋白表达被阻抑、ＰＫＣ活性明显降低的同时，ＰＫＡ活性则显著升高。结果提示：在人肺癌细胞中ＰＫＣα亚类和ｃＡＭＰ－ＰＫＡ通路显示出拮抗关系。ＰＫＣα和ＰＫＡ两套信号系统相互作用，共同调节人肺癌细胞的增殖和转化
To investigate the relationship between protein kinase Cα (PKCα) and its cyclic adenylate-protein kinase A (cAMP-PKA) signaling system, human lung cancer was treated with hexamethylene bisacetamide (HMBA) and PKC inhibitor Calphostin C, respectively. Cell LTEPa-2, the percentage of cell growth was counted and cAMP levels were determined. The PKCα gene expression was detected by dot blot hybridization and the activity of PKC and PKA kinase in human lung LTE Pa-2 cells expressing antisense PKCα was measured. The results showed that after treatment of human lung cancer LTE Pa-2 cells with 5 μmol/L HMBA for 3 days, cell proliferation was significantly suppressed, PKCα gene expression was decreased, and cAMP level was increased. When the 0.15 mg/LPKC inhibitor Calphostin C caused a decrease in the proliferation rate of human lung cancer cells, cAMP levels also increased. In human lung LTEPα-2 cells expressing antisense PKCα, when the expression of PKCα gene and protein was suppressed and PKC activity was significantly decreased, PKA activity was significantly increased. The results suggest that PKCα subtypes and cAMP-PKA pathway show an antagonistic relationship in human lung cancer cells. Interaction between PKCα and PKA Signaling Systems to Regulate Proliferation and Transformation of Human Lung Cancer Cells