Protection against human papillomavirus type 16-E7 oncogene-induced tumorigenesis by in vivo expression of dominant-negative c-jun

Molecular Carcinogenesis

Volumn 34, Issue 2, 2002, Pages 72-77

  Young, Matthew R ^a   Farrell, Linda ^b   Lambert, Paul ^b   Awasthi, Parirokh ^c   Colburn, Nancy H ^a  

^a NATIONAL CANCER INSTITUTE   (United States)

^b UNIVERSITY OF WISCONSIN MADISON   (United States)

^c SAIC FREDERICK INC   (United States)

Author keywords

Activator protein 1; Cancer prevention; Human papillomavirus type 16; TAM67; Tumor promotion

Indexed keywords

DIMETHYLBENZ[A]ANTHRACENE; GENE PRODUCT; PHORBOL ESTER DERIVATIVE; TRANSCRIPTION FACTOR AP 1;

ANIMAL TISSUE; ARTICLE; CANCER PREVENTION; CELL CYCLE; CELL PROLIFERATION; CONTROLLED STUDY; MOUSE; MOUTH CANCER; NEWBORN; NONHUMAN; ONCOGENE C JUN; PRIORITY JOURNAL; SKIN CARCINOGENESIS; TUMOR PROMOTION; UTERINE CERVIX CANCER; VIRUS CARCINOGENESIS; VIRUS ONCOGENE; WART VIRUS;

9,10-DIMETHYL-1,2-BENZANTHRACENE; ANIMALS; GENES, DOMINANT; GENES, JUN; MICE; MICE, TRANSGENIC; NEOPLASMS, EXPERIMENTAL; ONCOGENE PROTEINS, VIRAL; PAPILLOMAVIRIDAE; TETRADECANOYLPHORBOL ACETATE;

ANIMALIA; DNA VIRUSES; HUMAN PAPILLOMAVIRUS; HUMAN PAPILLOMAVIRUS TYPE 16; HUMAN PAPILLOMAVIRUS TYPES; HUMAN POLIOVIRUS 1; PAPILLOMAVIRUS; PAPOVAVIRIDAE;

EID: 0036275075     PISSN: 08991987     EISSN: None     Source Type: Journal    
DOI: 10.1002/mc.10050     Document Type: Article

References (22)

1. Squamous epithelial hyperplasia and carcinoma in mice transgenic for the human papillomavirus type 16 E7 oncogene
2. Human papillomavirus types 16 E6 and E7 contribute differently to carcinogenesis
3. Transgenic mice demonstrate AP-1 (activator protein-1) transactivation is required for tumor promotion
4. Expression of dominant negative Jun inhibits elevated AP-1 and NF-kappaβ transactivation and suppresses anchorage independent growth of HPV immortalized human keratinocytes
5. Induced expression of dominant negative cJun down regulates NFκβ and AP-1 target genes and suppresses tumor phenotype in human keratinocytes
6. Human papillomavirus type 16 E6 and E7 oncogenes abrogate radiation-induced DNA damage responses in vivo through p53-dependent and p53-independent pathways
7. The function and mechanism of promoters of carcinogenesis
8. Fluocinolone acetonide: A potent inhibitor of mouse skin tumor promotion and epidermal DNA synthesis
9. Influence of nonsteroid anti-inflammatory agents on protein synthesis and hyperplasia caused by a tumor promoter
10. Both conserved region 1 (CR1) and CR2 of the human papillomavirus type 16 E7 oncogene are required for induction of epidermal hyperplasia and tumor formation in transgenic mice
11. The human papillomavirus type 16 E7 gene product interacts with and trans-activates the AP1 family of transcription factors
12. Rb binds c-Jun and activates transcription
13. G1 events and regulation of cell proliferation
14. Ras activity and cyclin D1 expression: An essential mechanism of mouse skin tumor development
15. Transforming p21 ras mutants and c-Ets-2 activate the cyclin D 1 promoter through distinguishable regions
16. Transformation by ras modifies AP1 composition and activity
17. Overexpression of cyclin D1 in mouse skin carcinogenesis
18. Early overexpression of cyclin D1 protein in mouse skin carcinogenesis
19. Reduced skin tumor development in cyclin D1-deficient mice high-lights the oncogenic ras pathway in vivo
20. Cyclin D1 overexpression in mouse epidermis increases cyclin-dependent kinase activity and cell proliferation in vivo but does not affect skin tumor development
21. Transgenic studies with a keratin promoter-driven growth hormone transgene: Prospects for gene therapy
22. Crossspecies comparison of angiogenesis during the premalignant stages of squamous carcinogenesis in the human cervix and K14-HPV16 transgenic mice