TGF-β1 inhibition of c-myc transcription and growth in keratinocytes is abrogated by viral transforming proteins with pRB binding domains

Pietenpol, Jennifer A.; Stein, Roland; Morán, Elizabeth; Yaciuk, Peter; Schlegel, Richard; Lyons, Russette M.; Pittelkow, Mark R.; Münger, Karl; Howley, Peter M.; Moses, Harold L.

doi:10.1016/0092-8674(90)90188-k

Cited by 558 publications

(346 citation statements)

References 49 publications

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“…Speci®cally, we postulated that while the recruitment of c-Fos into speci®c AP-1 DNA-binding complexes was stimulated by serum-dependent signaling pathways (Felts et al, 1995), the functional activity of CAF was modulated by TGF-b1 (Felts et al, 1997). Although, as noted above, our data do not support a direct interaction between pRB and c-Fos, pRB has been implicated in TGF-b1 signaling pathways controlling both c-myc transcription in keratinocytes (Pietenpol et al, 1990(Pietenpol et al, , 1991 and junB transcription in epithelial cells (Giannini et al, 1997). It is therefore possible that pRB plays a similar role in TGF-b1-dependent transcriptional synergism in ®broblasts.…”

Section: Discussioncontrasting

confidence: 61%

The retinoblastoma gene family members pRB and p107 coactivate the AP-1-dependent mouse tissue factor promoter in fibroblasts

et al. 2000

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Serum-stimulation of quiescent mouse ®broblasts results in transcriptional activation of tissue factor (TF), the cellular initiator of blood coagulation. This requires the rapid entry of c-Fos into speci®c AP-1 DNA-binding complexes and can be strongly inhibited by the adenovirus E1A 12S gene product. In this study, we utilized a panel of E1A mutants de®cient in cellular protein binding to analyse the molecular basis for E1A inhibition of a minimal, c-Fos-dependent TF promoter/ reporter construct in mouse AKR-2B ®broblasts. Mutations which impaired binding of the retinoblastoma tumor suppressor protein family members pRB, p107, and p130 relieved E1A-mediated inhibition of transcription in response to serum-stimulation or c-Fos overexpression. Inhibition was restricted to the G 0 to G 1 transition, consistent with the speci®city of E1A for hypophosphorylated forms of RB proteins. Although E1A mutants de®cient in CBP/p300 binding retained the ability to inhibit TF transcription, deletion of the aminoterminal portion of the CBP/p300 interaction domain was required to permit rescue of TF promoter activity by coexpression of pRB. Moreover, ectopic p107 could e ectively substitute for pRB in relieving E1A-mediated repression. In primary mouse embryo ®broblasts, activity of the minimal AP-1-dependent TF promoter was suppressed in Rb 7/7 cells compared to parallel Rb +/7 and Rb +/+ transfectants. Ectopic expression of either pRB or p107 markedly enhanced TF promoter activity in Rb 7/7 ®broblasts. Collectively, these data imply that pRB and p107 can cooperate with c-Fos to activate TF gene transcription in ®broblasts and suggest a requirement for another, as yet unidenti®ed, E1A-binding protein. Oncogene (2000) 19, 3352 ± 3362.

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Section: Discussioncontrasting

confidence: 61%

The retinoblastoma gene family members pRB and p107 coactivate the AP-1-dependent mouse tissue factor promoter in fibroblasts

et al. 2000

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“…Expression of SV-LT can overcome a TGF-b1 mediated G 1 arrest in keratinocytes (Pietenpol et al, 1990) and mink lung epithelial cells (Laiho et al, 1990), and this e ect is dependent upon the pRbbinding domain. It is also probably independent of p53 binding, since the HPV E7 protein, which does not bind p53, has a similar e ect (Laiho et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Reversal of an antiestrogen-mediated cell cycle arrest of MCF-7 cells by viral tumor antigens requires the retinoblastoma protein-binding domain

Varma

Conrad

2000

Oncogene

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“…c-Myc expression is induced upon mitogenic signaling and peaks 3 ± 4 h after growth factor stimulation (Kelly et al, 1983). In cycling cells, c-Myc levels remain invariant and decline after induction of di erentiation (Einat et al, 1985;Pietenpol et al, 1990). Activation of c-myc is su cient to induce cell cycle entry in quiescent cells (Eilers et al, 1991).…”

Section: Abstract: C-myc; Cell Proliferation; Cell Cyclementioning

confidence: 99%

A genetic screen to identify genes that rescue the slow growth phenotype of c-myc null fibroblasts

et al. 2000

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TGF-β1 inhibition of c-myc transcription and growth in keratinocytes is abrogated by viral transforming proteins with pRB binding domains

Cited by 558 publications

References 49 publications

The retinoblastoma gene family members pRB and p107 coactivate the AP-1-dependent mouse tissue factor promoter in fibroblasts

The retinoblastoma gene family members pRB and p107 coactivate the AP-1-dependent mouse tissue factor promoter in fibroblasts

Reversal of an antiestrogen-mediated cell cycle arrest of MCF-7 cells by viral tumor antigens requires the retinoblastoma protein-binding domain

A genetic screen to identify genes that rescue the slow growth phenotype of c-myc null fibroblasts

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