Connexin 32 expression reduces malignant phenotype in human A549 adenocarcinoma cells: Implication of Src involvement
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- Published online on: November 1, 2006 https://doi.org/10.3892/or.16.5.1149
- Pages: 1149-1154
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Abstract
Recent evidence suggests that a member of the gap junction protein family, connexin (Cx) 32, acts as a tumor suppressor gene against lung adenocarcinoma. However, the precise mechanism remains unclear. In this study, we tried to explore the mechanism for the Cx32-dependent tumor-suppressive effect in lung adenocarcinoma. To perform this study, we established a stable clone of the human lung adenocarcinoma cell line, A549 in which the Cx32 gene was expressed. Cx32 expression in A549 cells reduced anchorage-independent growth and development of tumors in a xenograft model. Additionally, Cx32 induced contact inhibition of growth and reduced invasive activity in A549 cells. The tumor-suppressive effects of Cx32 depended on the inhibition of Src activity. These events were confirmed by an Src inhibitor (PP1) and siRNA for Cx32. These results suggest that the Cx32-dependent tumor-suppressive effect in A549 cells is explained by the inhibition of Src activity.