https://scholars.lib.ntu.edu.tw/handle/123456789/523950
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | MING-TSAN LIN | en_US |
dc.contributor.author | Lee R.-C. | en_US |
dc.contributor.author | PAN-CHYR YANG | en_US |
dc.contributor.author | Ho F.-M. | en_US |
dc.contributor.author | Kuo M.-L. | en_US |
dc.creator | Lin M.-T.;Lee R.-C.;Pan-Chyr Yang;Ho F.-M.;Kuo M.-L. | - |
dc.date.accessioned | 2020-12-02T02:36:07Z | - |
dc.date.available | 2020-12-02T02:36:07Z | - |
dc.date.issued | 2001 | - |
dc.identifier.issn | 0021-9258 | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-0035966107&doi=10.1074%2fjbc.M107829200&partnerID=40&md5=678271a9ac217afb71810c968d4144d0 | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/523950 | - |
dc.description.abstract | 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 (PGE 2) 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. | - |
dc.relation.ispartof | Journal of Biological Chemistry | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | Cells; Cloning; Ultraviolet radiation; Transfection; Enzymes; 2 morpholino 8 phenylchromone; celecoxib; cyclooxygenase 1; cyclooxygenase 2; DNA; n (2 cyclohexyloxy 4 nitrophenyl)methanesulfonamide; phosphatidylinositol 3 kinase inhibitor; prostaglandin E2; protein bcl 2; protein mcl 1; wortmannin; androstane derivative; antineoplastic agent; Culture Media, Serum Free; cyclooxygenase 2; DNA fragment; enzyme inhibitor; isoenzyme; MCL1 protein; oncoprotein; phosphatidylinositol 3 kinase; prostaglandin synthase; proto oncogene protein akt; Proto Oncogene Proteins; Proto Oncogene Proteins c bcl 2; proto-oncogene protein akt; tumor protein; vinblastine; apoptosis; article; cancer cell culture; cell death; cell survival; cll strain CL1.0; controlled study; enzyme assay; gene overexpression; genetic transfection; human; human cell; immunoblotting; lung adenocarcinoma; priority journal; prostaglandin synthesis inhibition; ultraviolet irradiation; adenocarcinoma; apoptosis; cell culture; culture medium; drug effect; genetics; lung tumor; metabolism; nick end labeling; pathophysiology; physiology; signal transduction; upregulation; vectors; 1-Phosphatidylinositol 3-Kinase; Adenocarcinoma; Androstadienes; Antineoplastic Agents, Phytogenic; Apoptosis; Cell Survival; Culture Media, Serum-Free; DNA Fragmentation; Enzyme Inhibitors; Human; In Situ Nick-End Labeling; Isoenzymes; Lung Neoplasms; Neoplasm Proteins; Prostaglandin-Endoperoxide Synthase; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-bcl-2; Signal Transduction; Support, Non-U.S. Gov't; Transfection; Tumor Cells, Cultured; Up-Regulation; Vinblastine | - |
dc.title | Cyclooxygenase-2 inducing Mcl-1-dependent survival mechanism in human lung adenocarcinoma CL1.0 cells: Involvement of phosphatidylinositol 3-kinase/Akt pathway | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.1074/jbc.M107829200 | - |
dc.identifier.pmid | 11585835 | - |
dc.identifier.scopus | 2-s2.0-0035966107 | - |
dc.relation.pages | 48997-49002 | - |
dc.relation.journalvolume | 276 | - |
dc.relation.journalissue | 52 | - |
item.fulltext | no fulltext | - |
item.cerifentitytype | Publications | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.grantfulltext | none | - |
item.openairetype | journal article | - |
crisitem.author.dept | Surgery | - |
crisitem.author.dept | Surgery-NTUH | - |
crisitem.author.dept | Internal Medicine | - |
crisitem.author.dept | Clinical Medicine | - |
crisitem.author.dept | Clinical Pharmacy | - |
crisitem.author.dept | Oncology | - |
crisitem.author.dept | Biomedical Electronics and Bioinformatics | - |
crisitem.author.dept | Internal Medicine-NTUH | - |
crisitem.author.orcid | 0000-0001-7313-7057 | - |
crisitem.author.orcid | 0000-0001-6330-6048 | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Electrical Engineering and Computer Science | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
顯示於: | 醫學系 |
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