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Effects of acetaldehyde on C-Jun/AP-...

Timmons, Sherry Rene.

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Effects of acetaldehyde on C-Jun/AP-1 expression in oral keratinocytes.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Effects of acetaldehyde on C-Jun/AP-1 expression in oral keratinocytes./
Author:	Timmons, Sherry Rene.
Description:	105 p.
Notes:	Source: Dissertation Abstracts International, Volume: 62-07, Section: B, page: 3125.
Contained By:	Dissertation Abstracts International62-07B.
Subject:	Health Sciences, Dentistry. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3018623
ISBN:	0493300392

Effects of acetaldehyde on C-Jun/AP-1 expression in oral keratinocytes.
Timmons, Sherry Rene.

Effects of acetaldehyde on C-Jun/AP-1 expression in oral keratinocytes. - 105 p.

Source: Dissertation Abstracts International, Volume: 62-07, Section: B, page: 3125.

Thesis (Ph.D.)--The University of Iowa, 2001.

Oral cancer is a significant health problem, particularly among individuals that ingest alcohol in combination with the use of tobacco products. The enhanced development of tobacco-initiated oral cancers by ethanol suggests that ethanol or one of its metabolites may act as a type of tumor promoter. Nevertheless, the mechanisms underlying the ability of ethanol to enhance oral carcinogenesis remain unclear. We hypothesize that acetaldehyde, the first metabolite of ethanol, may activate the expression and/or activity of Jun/AP-1 in oral keratinocytes analogous to the phorbol ester TPA and other tumor promoters in epidermal keratinocytes. We also hypothesize that acetaldehyde, and indirectly ethanol, may play a role during the progression stage of oral carcinogenesis by activating Jun/AP-1 expression and/or activity in transformed cells for the facilitation and/or maintenance of the malignant phenotype. To test this hypothesis, we treated HPV immortalized, non-tumorigenic human oral keratinocytes as well as transformed human oral keratinocytes, SCC-25, with acetaldehyde at various concentrations (10 muM--5 mM) and for various times (2--24h) and measured several parameters of Jun/AP-1 expression and function. Our results indicated that c-Jun mRNA and protein levels increased in the acetaldehyde treated cells compared to untreated control cells in both the non-tumorigenic and transformed cell lines. Moreover, Jun/AP-1 DNA binding activity was rapidly activated in the HPV-immortalized and transformed cells by acetaldehyde in a dose-dependent fashion. The increases in Jun protein and AP-1 DNA binding activity were accompanied by increased transactivation of an AP-1 responsive reporter construct transfected into the HPV-immortalized oral keratinocytes. The levels of acetaldehyde employed were minimally toxic to the HPV-immortalized cells as determined by MTT assays. Thus, acetaldehyde was found to activate the expression and activity of an oncogenic transcription factor in HPV-initiated cells as well as transformed malignant cells. Taken together, these results suggest that acetaldehyde may participate, at least in part, during both the promotion and progression stages of oral carcinogenesis.

ISBN: 0493300392Subjects--Topical Terms:

1019378
Health Sciences, Dentistry.

Effects of acetaldehyde on C-Jun/AP-1 expression in oral keratinocytes.
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100 1 $a Timmons, Sherry Rene. $3 1952614
245 1 0 $a Effects of acetaldehyde on C-Jun/AP-1 expression in oral keratinocytes.
300 $a 105 p.
500 $a Source: Dissertation Abstracts International, Volume: 62-07, Section: B, page: 3125.
500 $a Supervisors: Frederick E. Domann; Christopher A. Squier.
502 $a Thesis (Ph.D.)--The University of Iowa, 2001.
520 $a Oral cancer is a significant health problem, particularly among individuals that ingest alcohol in combination with the use of tobacco products. The enhanced development of tobacco-initiated oral cancers by ethanol suggests that ethanol or one of its metabolites may act as a type of tumor promoter. Nevertheless, the mechanisms underlying the ability of ethanol to enhance oral carcinogenesis remain unclear. We hypothesize that acetaldehyde, the first metabolite of ethanol, may activate the expression and/or activity of Jun/AP-1 in oral keratinocytes analogous to the phorbol ester TPA and other tumor promoters in epidermal keratinocytes. We also hypothesize that acetaldehyde, and indirectly ethanol, may play a role during the progression stage of oral carcinogenesis by activating Jun/AP-1 expression and/or activity in transformed cells for the facilitation and/or maintenance of the malignant phenotype. To test this hypothesis, we treated HPV immortalized, non-tumorigenic human oral keratinocytes as well as transformed human oral keratinocytes, SCC-25, with acetaldehyde at various concentrations (10 muM--5 mM) and for various times (2--24h) and measured several parameters of Jun/AP-1 expression and function. Our results indicated that c-Jun mRNA and protein levels increased in the acetaldehyde treated cells compared to untreated control cells in both the non-tumorigenic and transformed cell lines. Moreover, Jun/AP-1 DNA binding activity was rapidly activated in the HPV-immortalized and transformed cells by acetaldehyde in a dose-dependent fashion. The increases in Jun protein and AP-1 DNA binding activity were accompanied by increased transactivation of an AP-1 responsive reporter construct transfected into the HPV-immortalized oral keratinocytes. The levels of acetaldehyde employed were minimally toxic to the HPV-immortalized cells as determined by MTT assays. Thus, acetaldehyde was found to activate the expression and activity of an oncogenic transcription factor in HPV-initiated cells as well as transformed malignant cells. Taken together, these results suggest that acetaldehyde may participate, at least in part, during both the promotion and progression stages of oral carcinogenesis.
590 $a School code: 0096.
650 4 $a Health Sciences, Dentistry. $3 1019378
650 4 $a Health Sciences, Oncology. $3 1018566
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773 0 $t Dissertation Abstracts International $g 62-07B.
790 1 0 $a Domann, Frederick E., $e advisor
790 1 0 $a Squier, Christopher A., $e advisor
790 $a 0096
791 $a Ph.D.
792 $a 2001
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