Enhanced apoptosis under low serum conditions in human glioblastoma cells by connexin 43 (Cx43)

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Abstract
Connexin 43 (Cx43), a structural component of gap junctions, is believed to function as a tumor suppressor gene. Previously, we showed that expression of Cx43 suppresses cell proliferation and tumorigenicity of human glioblastoma cells [Huang et al., Cancer Res 58:5089–5096, 1998] and enhances apoptosis in response to chemotherapeutic agents [Huang et al., Int J Cancer 92:130–138, 2001]. In the present study, we demonstrated that expression of Cx43 in human glioblastoma cells potentiated an apoptotic program under low‐serum conditions. The Cx43‐mediated effect was coupled with a decreased expression of the specific apoptosis‐inhibitor bcl‐2. Overexpression of bcl‐2 in Cx43‐transfected cells conferred resistance to apoptosis induced under low‐serum conditions, suggesting that the Cx43‐mediated apoptosis under low‐serum conditions is regulated, in part, through the downregulation of bcl‐2 expression. Furthermore, application of the phosphatidylinositol‐3′‐OH kinase inhibitor LY294002 specifically induced apoptosis in Cx43‐transfected cells. Our results demonstrate a new role of Cx43 in the mediation of apoptosis under low serum conditions.