Genetic complementation to non-tumorigenicity in cervical-carcinoma cells correlates with alterations in AP-1 composition

Soto, Ubaldo; Denk, Claudia; Finzer, Patrick; Hutter, K.‐J.; Hausen, Harald zur; Rösl, Frank

doi:10.1002/(sici)1097-0215(20000615)86:6<811::aid-ijc9>3.0.co;2-j

Cited by 42 publications

(49 citation statements)

References 19 publications

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“…Notably, similar to non-malignant cells, HPV16-positive CaSki cells expressed high/low levels of Net/c-Fos. This was interesting in the context of our previous observation that in contrast to SiHa or SW756, CaSki cells were able to complement highly tumorigenic HeLa cells to a non-malignant phenotype after somatic cell hybridization (8). Moreover, a potential link between Net and the nucleosomal organization of the c-fos promoter was provided by the fact that its binding to native chromatin could be exclusively detected in non-malignant cells when formaldehyde cross-linked lysates were analyzed (Fig.…”

Section: Discussionmentioning

confidence: 77%

“…The decision, however, which target genes finally turns out to be induced, is apparently depending on AP-1 composition (47). For HPV-positive human cells, AP-1 is part of an intracellular surveillance network determining not only the in vivo phenotype but also the sensitivity/response against growth inhibitory cytokines and chemokines (1,7,8).…”

Section: Discussionmentioning

confidence: 99%

“…Both HPV16- positive SiHa as well as HPV18-positive SW756 cells exhibited low levels of Net, whereas c-fos transcription was highly upregulated. Exceptional for cervical carcinoma cells, c-fos was weakly transcribed in HPV16-positive CaSki cells (8). Notably, examining these cells by RT-PCR and Western blot analysis, a high amount of Net could be discerned (Fig.…”

Section: Diminished Net Expression In Tumorigenic Cells: Loss Of Reprmentioning

confidence: 92%

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Loss of Net as Repressor Leads to Constitutive Increased c-fos Transcription in Cervical Cancer Cells

Riggelen¹,

Buchwalter²,

Soto³

et al. 2005

Journal of Biological Chemistry

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We have investigated the expression of c-fos in cervical carcinoma cells and in somatic cell hybrids derived therefrom. In malignant cells, c-fos was constitutively expressed even after serum starvation. Dissection of the c-fos promoter showed that expression was mainly controlled by the SRE motif, which was active in malignant cells, but repressed in their non-malignant counterparts. Constitutive SRE activity was not mediated by sustained mitogen-activated protein kinase activity but because of inefficient expression of the ternary complex factor Net, which was either very low or even barely discernible. Chromatin immunoprecipitation assays re-

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Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Diminished Net Expression In Tumorigenic Cells: Loss Of Reprmentioning

confidence: 92%

See 1 more Smart Citation

Loss of Net as Repressor Leads to Constitutive Increased c-fos Transcription in Cervical Cancer Cells

Riggelen¹,

Buchwalter²,

Soto³

et al. 2005

Journal of Biological Chemistry

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“…Overexpression of the proto-oncogene c-fos has been demonstrated in different cancers and is known to correlate with the carcinogenesis, for example, the extent of c-fos expression is associated with the clinical degree and progression of pancreatic cancer (Lee and Charalambous 1994). Soto et al reported that increased amounts of c-fos and low level of fra-1 can be discerned in cervical carcinoma cell lines such as Hela, SW756 and SiHa (Rösl et al 1997;Soto et al 1999Soto et al , 2000Talora et al 2002). Gree et al also found transfection of c-fos into murine papilloma cell lines expressed an activated Ha-ras oncogene and resulted in the malignant conversion of these cells (Greenhalgh and Yuspa 1988).…”

Section: Discussionmentioning

confidence: 99%

Growth Inhibitory Effect of the Ternary Complex Factor Net on Human Pancreatic Carcinoma Cell Lines

Zhu

et al. 2008

Tohoku J. Exp. Med.

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Pancreatic carcinoma is one of the most aggressive malignancies and carries the most dismal prognoses of all cancers. A better understanding of the genes involving in tumor development may allow us to tackle this rapidly progressive disease. The Net gene belongs to the ternary complex transcription factor (TCF) family and is regulated by the Ras/mitogen-activited protein kinase-signaling pathway. Under basal conditions, Net shows strong represssing function on transcription of proto-oncogene gene c-fos. Moreover, the lower expression of Net has been noted in some carcinoma cells, such as cervical cancer. To study the effect of Net on c-fos expression and its potential role in the growth of pancreatic carcinoma, we developed a recombinant plasmid, a pEGFP-N1-Net, which codes for Net-EGFP fusion proteins, and stably transfected it into BxPC-3 human pancreatic carcinoma cells. Using stable transformants, we were able to show that overexpression of Net decreased the expression of c-fos and inhibited pancreatic cancer cell proliferation. Cell cycle analysis demonstrated that Net overexpression inhibited cell cycle progression. These findings suggested that loss of Net repression could augment c-fos expression and further trigger neoplastic cell proliferation, which was involved in the pathogenesis of pancreatic cancer. Therefore, Net might be a potential target for the treatment of c-fos-positive pancreatic cancer.

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“…The interruption of this cellular control in infected basal layer cells emerges as a prime factor in cell immortalization, but also in malignant conversion (reviewed in zur Hausen, 1994bHausen, , 1996. Whereas events linked to immortalization seem to result from modi®cations of intracellular signaling cascades, in malignant conversion intercellular regulatory mechanisms are a ected, rendering the malignant cells nonresponsive to TNF-a mediated changes in the heterodimerization of the AP-1 complex (Soto et al, 1993(Soto et al, , 2000 and reducing their ability to induce endogenous interferon-b synthesis (Bachmann et al, 2001).…”

Section: Mechanisms By Which Viruses Contribute To Cancermentioning

confidence: 99%

Oncogenic DNA viruses

Hausen

2001

Oncogene

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Genetic complementation to non-tumorigenicity in cervical-carcinoma cells correlates with alterations in AP-1 composition

Cited by 42 publications

References 19 publications

Loss of Net as Repressor Leads to Constitutive Increased c-fos Transcription in Cervical Cancer Cells

Loss of Net as Repressor Leads to Constitutive Increased c-fos Transcription in Cervical Cancer Cells

Growth Inhibitory Effect of the Ternary Complex Factor Net on Human Pancreatic Carcinoma Cell Lines

Oncogenic DNA viruses

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