Anticancer Research vol. 30, no. 7, pp. 2823 - 2830
SCI; SCIE; SCOPUS
Background: Human A3 adenosine receptor (A3AR) plays an essential role in several physiopathological processes. Thus far, A 3AR-selective ligands have been evaluated as anti-inflammation and anticancer therapeutic agents. Among these ligands, truncated thio-Cl-IB-MECA is a newly reported antagonist, and its function has not been studied. Materials and Methods: Cell viability was measured by MTS assay. Cell cycle progression was analysed by propidium iodide (PI) flow cytometric assay. The apoptotic effects were investigated by Hoechst staining and annexin V-FITC/PI staining. The signal-transduction mechanism was explored by Western blot. Results: Truncated thio-Cl-IB-MECA induced the growth arrest of T24 cells at sub-G 1 phase and provoked apoptosis but not necrosis. Apoptotic death was mediated by the activation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK). Conclusion: Since truncated thio-Cl-IB-MECA induces anti-proliferation and apoptotic effects via ERK and JNK activation, it may function as an anticancer agent in human bladder cancer cells.