A dominant negative c-jun specifically blocks okadaic acid-induced skin tumor promotion

Cancer Research

Volumn 62, Issue 11, 2002, Pages 3044-3047

  Thompson, Eric J ^a   Bowden, G Tim ^a   MacGowan, Jacalyn ^a   Young, Matthew R ^b   Colburn, Nancy ^b  

^a UNIVERSITY OF ARIZONA   (United States)

^b NATIONAL CANCER INSTITUTE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

7,12 DIMETHYLBENZ[A]ANTHRACENE; OKADAIC ACID; PHORBOL ESTER; PHOSPHOPROTEIN PHOSPHATASE; STRESS ACTIVATED PROTEIN KINASE; TOSYLARGININE METHYL ESTER; TRANSCRIPTION FACTOR AP 1;

ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL PROLIFERATION; CONTROLLED STUDY; ENZYME ACTIVITY; GENE EXPRESSION; GENETIC TRANSCRIPTION; MOUSE; NONHUMAN; NORTHERN BLOTTING; NUCLEOTIDE SEQUENCE; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; REGULATORY MECHANISM; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; SIGNAL TRANSDUCTION; SKIN CARCINOGENESIS; SKIN TUMOR; TRANSCRIPTION INITIATION;

9,10-DIMETHYL-1,2-BENZANTHRACENE; ANIMALS; CARCINOGENS; ENZYME INDUCTION; MATRIX METALLOPROTEINASE 3; MICE; MICE, INBRED DBA; MICE, INBRED ICR; MICE, TRANSGENIC; OKADAIC ACID; PEPTIDE FRAGMENTS; PROTO-ONCOGENE PROTEINS C-JUN; SKIN; SKIN NEOPLASMS; TRANSCRIPTION FACTOR AP-1;

EID: 0036606621     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (27)

1. Okadaic acid: An additional non-phorbol-12-tetradecanoate-13-acetate-type tumor promoter
2. Cyanobacterial toxins: Removal during drinking water treatment, and human risk assessment
3. Inhibition of protein phosphatases by microcystins and nodularin associated with hepatotoxicity
4. Protein phosphatase 2A: A highly regulated family of serine/threonine phosphatases implicated in cell growth and signalling
5. Mechanisms of action of okadaic acid class tumor promoters on mouse skin
6. Activation of AP-1 by okadaic acid in mouse keratinocytes associated with hyperphosphorylation of c-jun
7. AP-1 in cell proliferation and survival
8. Okadaic acid-stimulated TRE binding activity in a papilloma-producing mouse keratinocyte cell line involves increased AP-1 expression
9. Extracellular signal-regulated kinase 1/2-mediated phosphorylation of JunD and FosB is required for okadaic acid-induced activator protein 1 activation
10. Okadaic acid induces the expression of both early and secondary response genes in mouse keratinocytes
11. AP-1 in mouse development and tumorigenesis
12. AP1/jun function is differentially induced in promotion-sensitive and resistant JB6 cells
13. Blocking of tumor promoter-induced AP-1 activity inhibits induced transformation in JB6 mouse epidermal cells
14. Constitutive AP-1 DNA binding and transactivating ability of malignant but not benign mouse epidermal cells
15. Antitumor promotion by phenolic antioxidants: Inhibition of AP-1 activity through induction of Fra expression
16. Suppression of oncogene-induced transformation by a deletion mutant of c-jun
17. A dominant negative mutant of jun blocking 12-O-tetradecanoylphorbol-13-acetate-induced invasion in mouse keratinocytes
18. Stable expression of a c-JUN deletion mutant in two malignant mouse epidermal cell lines blocks tumor formation in nude mice
19. Transgenic mice demonstrate AP-1 (activator protein-1) transactivation is required for tumor promotion
20. AP-1 transcriptional activity requires both T-cell receptor-mediated and co-stimulatory signals in primary T lymphocytes
21. Altered expression of insulin-like growth factor I and its receptor during multistage carcinogenesis in mouse skin
22. Inflammatory versus proliferative processes in epidermis. Tumor necrosis factor α induces K6b keratin synthesis through a transcriptional complex containing NFκB and C/EBPβ
23. Cross-family dimerization of transcription factors Fos/Jun and ATF/CREB alters DNA binding specificity
24. Cross-coupling of the NF-κB p65 and Fos/Jun transcription factors produces potentiated biological function
25. Transformation nonresponsive cells owe their resistance to lack of p65/nuclear factor-κB activation
26. Induced expression of dominant-negative c-jun down-regulates NFκB and AP-1 target genes and suppresses tumor phenotype in human keratinocytes
27. Essential role of tumor necrosis factor α (TNF-α) in tumor promotion as revealed by TNF-α-deficient mice