Abstract:
:A1, a member of the Bcl-2 gene family, was originally identified as a hemopoietic-specific early response gene. Later it was found that A1 was overexpressed in human stomach cancer tissues and was induced by tumor necrosis factor-alpha (TNF-alpha) in human vascular endothelial cells. However, its expression in human cancer cells has not been well characterized. In the present study, we examined the expression of A1, as well as the antioxidant manganous superoxide dismutase (MnSOD), in four human thyroid carcinoma cell lines, two human pancreatic carcinoma cell lines, and two human prostate carcinoma cell lines. A1 mRNA was expressed in all four thyroid carcinoma cell lines. TNF-alpha induced A1 in a time- and dose-dependent manner. In contrast, A1 mRNA was not detectable in the pancreatic and prostate carcinoma cell lines in the presence or absence of TNF-alpha. However, TNF-alpha induced manganous superoxide dismutase (MnSOD) mRNA in all the cell lines tested. Furthermore, an agonist antibody to the p55 TNF-alpha receptor induced A1, but the agonist antibody against p75 TNF-alpha receptor did not have this effect. The results indicate that A1 is expressed in human thyroid carcinoma cells and TNF-alpha induces A1 through the p55 TNF-alpha receptor-mediated pathway.
journal_name
Oncol Resjournal_title
Oncology researchauthors
Pang XP,Hershman JM,Karsan Asubject
Has Abstractpub_date
1997-01-01 00:00:00pages
623-7issue
11-12eissn
0965-0407issn
1555-3906journal_volume
9pub_type
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journal_title:Oncology research
pub_type: 杂志文章
doi:10.3727/000000006783981206
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journal_title:Oncology research
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journal_title:Oncology research
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journal_title:Oncology research
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journal_title:Oncology research
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journal_title:Oncology research
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abstract::Liver injury is often observed in various pathological conditions including posthepatectomy state and cancer chemotherapy. It occurs mainly as a consequence of the combined necrotic and apoptotic types of cell death. In order to study liver/hepatocyte injury by the necrotic type of cell death, we studied signal-regula...
journal_title:Oncology research
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journal_title:Oncology research
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doi:10.3727/096504013X13786659070316
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journal_title:Oncology research
pub_type: 杂志文章,评审
doi:10.3727/096504008786111383
更新日期:2008-01-01 00:00:00
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journal_title:Oncology research
pub_type: 杂志文章
doi:
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journal_title:Oncology research
pub_type: 杂志文章
doi:
更新日期:2000-01-01 00:00:00
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journal_title:Oncology research
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doi:10.3727/096504017X15017209042610
更新日期:2018-04-10 00:00:00
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journal_title:Oncology research
pub_type: 杂志文章
doi:10.3727/096504011x13021877989711
更新日期:2011-01-01 00:00:00
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journal_title:Oncology research
pub_type: 杂志文章
doi:10.3727/096504020X15942028641011
更新日期:2020-07-08 00:00:00
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journal_title:Oncology research
pub_type: 杂志文章
doi:
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journal_title:Oncology research
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doi:10.3727/096504013X13685487925095
更新日期:2013-01-01 00:00:00
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journal_title:Oncology research
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journal_title:Oncology research
pub_type: 杂志文章
doi:
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journal_title:Oncology research
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journal_title:Oncology research
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journal_title:Oncology research
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abstract::Aclacinomycin (ACR) is an anthracycline anticancer drug that shows marked effects in Adriamycin (ADM)-resistant tumors. ADM, however, is not effective against ACR-resistant tumor cells. When tumor cells acquire resistance to ACR, though the resistance is not easily acquired, they show strong cross-resistance to ADM. T...
journal_title:Oncology research
pub_type: 杂志文章
doi:
更新日期:1995-01-01 00:00:00
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journal_title:Oncology research
pub_type: 杂志文章
doi:
更新日期:1998-01-01 00:00:00
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journal_title:Oncology research
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journal_title:Oncology research
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