Epac1 is involved in cell cycle progression in lung cancer through PKC and Cx43 regulation

Epac1 通过 PKC 和 Cx43 调节参与肺癌细胞周期进程

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作者:Qian Sun, Dai Wang, Ganghao Ai, Longben Tian, Long Zhao, Renzhen Chen, Kai Wang, Dongbei Guo, Youliang Yao, Wenzhi Liu, XIangyu Kong, Xiaoxuan Chen, Yongxing Zhang

Conclusion

Normal Epac1 expression may suppress lung cancer occurrence and metastasis, and its downregulation is involved in cell cycle progression in lung cancer through PKC and Cx43 regulation.

Material and methods

Epac1, Cx43 (46 cases) and PKC, AKAP95 (45 cases) immunoexpression levels were determined in tissue samples of lung cancer and in 12 samples of neighboring para-carcinoma specimens by the PV-9000 Two-step immunohistochemical technique.

Methods

Epac1, Cx43 (46 cases) and PKC, AKAP95 (45 cases) immunoexpression levels were determined in tissue samples of lung cancer and in 12 samples of neighboring para-carcinoma specimens by the PV-9000 Two-step immunohistochemical technique.

Results

The percentage of Epac1 positive samples was significantly lower in lung cancer tissue than in neighboring para-carcinoma specimens (37% vs. 83.3%, p < 0.05); the difference in PKC immunoreactivity was not significant (64.4% vs. 91.7%). Epac1 expression was associated with the degree of malignancy and lymph node metastasis (P < 0.05), but not with histological type (P > 0.05), whereas PKC expression was not related to these parameters. Interestingly, Epac1 expression was correlated with PKC and Cx43 expression. Moreover, PKC expression was correlated with AKAP95 expression.

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