A(3) Adenosine Receptor Antagonist, Truncated Thio-Cl-IB-MECA, Induces Apoptosis in T24 Human Bladder Cancer Cells
- Authors
- Kim, Heejong; Kang, Jeong Woo; Lee, Sojung; Choi, Won Jun; Jeong, Lak Shin; Yang, Young; Hong, Jin Tae; Yoon, Do Young
- Issue Date
- Jul-2010
- Publisher
- INT INST ANTICANCER RESEARCH
- Keywords
- A3 adenosine receptor; A3AR antagonist; Apoptosis; Truncated thio-Cl-IB-MECA
- Citation
- ANTICANCER RESEARCH, v.30, no.7, pp 2823 - 2830
- Pages
- 8
- Journal Title
- ANTICANCER RESEARCH
- Volume
- 30
- Number
- 7
- Start Page
- 2823
- End Page
- 2830
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13179
- ISSN
- 0250-7005
1791-7530
- Abstract
- Background: Human A(3) adenosine receptor (A(3)AR) plays an essential role in several plzysiopathological processes. Thus far, A(3)AR-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.
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