Effects of a dominant-negative inhibitor of c-jun in lung cancer cell lines

Brown, Powel H.; Seigfried, J; Chen, T; Szabó, Edit; Sabichi, Anita L.; Preis, L.; Birrer, M. J.

doi:10.1016/0169-5002(94)90669-6

Cited by 24 publications

(33 citation statements)

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“…Along with overexpression comes an increase in AP-1 speci®c DNA binding and transcriptional regulatory activity ± properties consistent with an oncogenic mechanism utilizing both of these activities. Concordant with this hypothesis, mutations that a ect DNA binding or transcriptional activation activity abolish transforming activity (Brown et al, 1993;Granger-Schnarr et al, 1992;Lloyd et al, 1991). Quite strikingly, a completely di erent e ect is seen in avian cells.…”

Section: Discussionmentioning

confidence: 75%

“…In rodent cells, transformation resulting from overexpression of c-Jun has been correlated to increases in DNA binding and transcriptional regulatory activity (SchuÈ tte et al, 1989). Indeed, mutations which a ect either DNA binding or transcriptional activation abolish transforming activity (Alani et al, 1991;Brown et al, 1993;GrangerSchnarr et al, 1992;Lloyd et al, 1991). These results are in striking contrast to what has been observed in response to Jun induced transformation of avian cells.…”

Section: Introductionmentioning

confidence: 99%

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Directed mutation of the basic domain of v-Jun alters DNA binding specificity and abolishes its oncogenic activity in chicken embryo fibroblasts

Basso

Briggs²,

Findlay³

et al. 2000

Oncogene

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Section: Discussionmentioning

confidence: 75%

Section: Introductionmentioning

confidence: 99%

Directed mutation of the basic domain of v-Jun alters DNA binding specificity and abolishes its oncogenic activity in chicken embryo fibroblasts

Basso

Briggs²,

Findlay³

et al. 2000

Oncogene

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“…An eightfold difference in AP-1 activity was found between these two cell lines, confirming our gel shift assays. We then analysed the contribution of AP-1 pathway to IL-8 gene regulation by transfecting two inhibitors of AP-1 (JDP-1 and JDP-2) (Wardell et al, 2002) and a dominant-negative c-Jun mutant (Tam67) (Brown et al, 1993) (Figure 6b). These three inhibitors reduced by about 60-70% IL-8 promoter activity.…”

Section: Resultsmentioning

confidence: 99%

Mechanisms underlying differential expression of interleukin-8 in breast cancer cells

et al. 2004

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We have recently reported that interleukin-8 (IL-8) expression was inversely correlated to estrogen receptor (ER) status and was overexpressed in invasive breast cancer cells. In the present study, we show that IL-8 overexpression in breast cancer cells involves a higher transcriptional activity of IL-8 gene promoter. Cloning of IL-8 promoter from MDA-MB-231 and MCF-7 cells expressing high and low levels of IL-8, respectively, shows the integrity of the promoter in both cell lines. Deletion and site-directed mutagenesis of the promoter demonstrate that NF-jB and AP-1 and to a lesser extent C/EBP binding sites play a crucial role in the control of IL-8 promoter activity in MDA-MB-231 cells. Knockdown of NF-jB and AP-1 activities by adenovirusmediated expression of an NF-jB super-repressor and RNA interference, respectively, decreased IL-8 expression in MDA-MB-231 cells. On the contrary, restoration of Fra-1, Fra-2, c-Jun, p50, p65, C/EBPa and C/EBPb expression levels in MCF-7 cells led to a promoter activity comparable to that observed in MDA-MB-231 cells. Our data constitute the first extensive study of IL-8 gene overexpression in breast cancer cells and suggest that the high expression of IL-8 in invasive cancer cells requires a complex cooperation between NF-jB, AP-1 and C/EBP transcription factors.

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“…Inhibition of AP-1 activity in transformed JB6 RT101 cells caused reversion of the tumor phenotype (Dong et al, 1995a, b;Lavrovsky et al, 1996). In light of AP-1 activation by tumor promoters and the important role of induced AP-1 activity in tumor promoter-induced transformation, the u.v.-induced AP-1 response may have an important role in tumor promotion (Dong et al, 1994a(Dong et al, , 1995aBrown et al, 1993;Kerr et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Signal transduction through atypical PKCs, but not the EGF receptor, is necessary for UVC-induced AP-1 activation in immortal murine cells

Huang

Dong

1997

Oncogene

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The exposure of mammalian cells to ultraviolet (u.v.) irradiation leads to activation of transcription factors, such as AP-1 and NFkB. It is postulated that the EGF receptor but not protein kinase C (PKC) is the major membrane mediator in UVC-induced signal transduction. We demonstrate here that the antisense oligonucleotides of PKCz and the dominant negative mutant of PKCl/i as well as dominant negative PKCz markedly blocked UVC-induced AP-1 activity. In contrast, UVC-induced AP-1 activity in cells devoid of the EGF receptor (B82), is not signi®cantly di erent from that of the stable transfectants with a kinase-de®cient EGF receptor (B82M721), or wild-type EGF receptor (B82L). This was found at all UVC irradiation doses and time courses studied, while high levels of EGF-induced AP-1 activity were observed in B82L cells but not in B82 cells. This evidence strongly suggests that atypical PKCs, but not the EGF receptor, is necessary for UVC-induced AP-1 activation in JB6 and B82 cells.

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Effects of a dominant-negative inhibitor of c-jun in lung cancer cell lines

Cited by 24 publications

References 0 publications

Directed mutation of the basic domain of v-Jun alters DNA binding specificity and abolishes its oncogenic activity in chicken embryo fibroblasts

Directed mutation of the basic domain of v-Jun alters DNA binding specificity and abolishes its oncogenic activity in chicken embryo fibroblasts

Mechanisms underlying differential expression of interleukin-8 in breast cancer cells

Signal transduction through atypical PKCs, but not the EGF receptor, is necessary for UVC-induced AP-1 activation in immortal murine cells

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