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Medulloblastoma (MB) is one of the most common malignant brain tumors ofchildhood and is associated with a poor prognosis. Gap-junctional intercellularcommunication (GJIC) is an important mode for cell-to-cell communication. DysfunctionalGJIC is exhibited in most cancer cells. There is significant evidence that GJICis important in at least some prodrug/suicide gene systems by augmenting the bystandereffect (BE). GJIC is made up of connexins (Cxs), among which Cx43 is present inmost tissues. Bcl-2, an important apoptosis blocker, is closely associated withthe sensitivity to anticancer drugs. Our study showed that dibutyryl cyclic adenosinemonophosphate (db-cAMP) upregulated the Cx43 expression and GJIC function in Daoymedulloblastoma cells. It directly enhanced the BE using a herpes simplex virusthymidine kinase (HSV‑tk)/ganciclovir (GCV) system, which was blocked by a Cx43inhibitor. In addition, db-cAMP increased the cytotoxicity of temozolomide andteniposide, possibly by downregulating the Bcl-2 expression and inducing apoptosis.Taken together, we demonstrated the beneficial effect of db-cAMP in treating medulloblastomadepending on the upregulation of BE and chemosensitivity through Cx43 and Bcl-2-mediatedpathways.

Action of db-cAMP on the bystander effect and chemosensitivity through connexin 43 and Bcl-2-mediated pathways in medulloblastoma cells