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J. Biol. Chem., Vol. 276, Issue 52, 48997-49002, December 28, 2001
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From the Cyclooxygenase 2 (COX-2) has been reported to be
commonly expressed in advanced stages of human lung adenocarcinoma. In
this study, the COX-2 constitutive expression vector was transfected into a human lung adenocarcinoma cell line CL1.0 and several clones were obtained which stably expressed COX-2. These COX-2-overexpressed clones demonstrated remarkable resistance to apoptosis induced by
Ultraviolet B (UVB) irradiation, vinblastine B (VBL) cell lymphoma-2 (Bcl-2), or other anti-cancer drugs. To understand how COX-2
prevents apoptosis, the investigators examined the expression level of Bcl-2 family members. Mcl-1, but not other Bcl-2 members, was significantly up-regulated by COX-2 transfection or prostaglandin E2 (PGE2) treatment. Treatment of
COX-2-overexpressed cells (cox-2/cl.4) with two specific COX-2
inhibitors, NS-398 and celecoxib, caused an effective reduction of the
increased level of Mcl-1. These data suggest that the expression level
of Mcl-1 is tightly regulated by COX-2. Moreover, transfection of
cox-2/cl.4 cells with antisense Mcl-1 enhanced apoptosis induced by UVB
irradiation, revealing that Mcl-1 plays a crucial role in cell survival
activity mediated by COX-2. Furthermore, COX-2 transfection or
PGE2 treatment evidently activated the
phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Inhibition of the PI3K pathway by LY294002 or wortmannin effectively attenuated the increased level of Mcl-1 induced by COX-2 or
PGE2. Blocking the PI3K activity with a dominant-negative
vector, DN-p85, also greatly diminished the level of Mcl-1 and enhanced
UVB-elicited cell death in cells transfected by COX-2. In a similar
way, LY294002 inhibited cell survival and Mcl-1 level in
PGE2-treated CL1.0 cells. These findings suggest that COX-2
promotes cell survival by up-regulating the level of Mcl-1 by
activating the PI3K/Akt-dependent pathway.
Cyclooxygenase-2 Inducing Mcl-1-dependent
Survival Mechanism in Human Lung Adenocarcinoma CL1.0
Cells
INVOLVEMENT OF PHOSPHATIDYLINOSITOL 3-KINASE/Akt PATHWAY*
,
, and Department of Surgery, National Taiwan
University Hospital, Taipei 100, Taiwan, § Laboratory of
Molecular and Cellular Toxicology, Institute of Toxicology, College of
Medicine, National Taiwan University, Taipei 100, Taiwan,
¶ Department of Internal Medicine, National Taiwan University
Hospital, Taipei 100, Taiwan, and Tao-Yuan General Hospital,
Taoyuan 330, Taiwan
*
This research was supported by the National Science Council
of the Republic of China, Taiwan under Contracts NSC-89-2316-B-002-031 and NSC 89-2320-B-002-259.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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