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Adenosine induces apoptosis through TNFR1/RIPK1/P38 axis in colon cancer cells.

Abstract：

:Adenosine, a metabolite of ATP, ubiquitously exists in a wide range of organs and tissues. We previously reported that adenosine was implicated in apoptosis in many cancer cells by extrinsic and/or intrinsic pathways. Here, we found that adenosine suppresses the cell growth by induction of apoptosis of human colonic cancer cells through a novel mechanism. Adenosine suppresses the cell growth of human SW620 and SW480 colon cells in an adenosine transporter and adenosine kinase dependent manner. Moreover, the cell growth suppression is induced by apoptosis through activation of caspase-3 and PARP, and accumulation of ROS in cells. Importantly, we found that adenosine increases the expression of TNFR1 and RIPK1 and the phosphorylation of p38. Knockdown of TNFR1 or RIPK1 impairs the activation of p38, blocks the cleavage of PARP, and provides partially, yet significantly protection from cell death, including reducing the ROS generation in the colon cancer cells. These results indicate that a TNFR1/RIPK1/P38 axis is present in adenosine-induced apoptosis of colonic cancer cells. This axis triggers apoptosis and plays crucial roles in relay of the death signaling. Our study also provides additional experimental evidence for adenosine as a potent therapeutic drug in cancer therapy.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Yu S,Hou D,Chen P,Zhang Q,Lv B,Ma Y,Liu F,Liu H,Song EJ,Yang D,Liu J

doi

10.1016/j.bbrc.2015.03.103

subject

Has Abstract

pub_date

2015-05-08 00:00:00

pages

759-65

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(15)00559-8

journal_volume

460

pub_type

杂志文章

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