Induction of senescence by adenosine suppressing the growth of lung cancer cells.

Abstract

Extracellular adenosine is well reported to suppress tumor growth by induction of apoptosis. However, in this study we found that adenosine treatment results in cellular senescence in A549 lung cancer cells both in vitro and in vivo; adenosine induces cell cycle arrest and senescence in a p53/p21 dependent manner; adenosine elevates the level of phosphor-γH2AX, pCHK2 and pBRCA1, the markers for prolonged DNA damage response which are likely responsible for initiating the cellular senescence. Our study first demonstrates that adenosine suppresses growth of cancer cells by inducing senescence and provides additional evidence that adenosine could act as an effective anticancer agent for targeted cancer therapy.

• Authors: Dongqin Yang, Junyao Song, Lijun Wu, Yunfang Ma, Chunhua Song, Sinisa Dovat, Tomoyuki Nishizaki, Jie Liu
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 440 Issue 1 Pg. 62-7 (Oct 11 2013) ISSN: 1090-2104 [Electronic] United States
• PMID: 24051088 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2013 Elsevier Inc. All rights reserved.

Chemical References

• Antineoplastic Agents
• Cyclin-Dependent Kinase Inhibitor p21
• Tumor Suppressor Protein p53
• Adenosine

Topics

• Adenosine (pharmacology, therapeutic use)
• Animals
• Antineoplastic Agents (pharmacology, therapeutic use)
• Cell Cycle Checkpoints (drug effects)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Cellular Senescence (drug effects)
• Cyclin-Dependent Kinase Inhibitor p21 (metabolism)
• Female
• Humans
• Lung (drug effects, pathology)
• Lung Neoplasms (drug therapy, pathology)
• Mice
• Mice, Inbred BALB C
• Mice, Nude
• Tumor Suppressor Protein p53 (metabolism)