Retinoic Acid Promotes Ubiquitination and Proteolysis of Cyclin D1 during Induced Tumor Cell Differentiation

Spinella, Michael J.; Freemantle, Sarah J.; Sekula, David; Chang, Jeffrey H.; Christie, Allison J.; Dmitrovsky, Ethan

doi:10.1074/jbc.274.31.22013

Cited by 148 publications

(185 citation statements)

References 49 publications

(73 reference statements)

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“…This pattern became apparent by day 3, which corresponded to the start of growth inhibition. These results are consistent with other reports which show that RA causes hypophosphorylation of RB in various cell lines (Matsuo and Thiele, 1998;Naderi and Blomho , 1999;Seewaldt et al, 1999;Spinella et al, 1999;Sueoka et al, 1999;Teixeira and Pratt, 1997;Watanabe et al, 1999;Wilcken et al, 1996;Zancai et al, 1998). For example, Wilcken et al (1996) reported hypophosphorylation of RB in T-47D breast cancer cells upon RA treatment.…”

Section: Discussionsupporting

confidence: 82%

“…Matsuo and Thiele (1998) reported a complete down-regulation of G-1 cyclin/cdk activity and hypophosphorylated RB protein in SMS-KCNR human neuroblastoma cells. Spinella et al (1999) found that in the human embryonic carcinoma cell line NT2/D1, RA caused a progressive decline in cyclin D1 and hypophosphorylation of RB. Finally, Naderi and Blomho (1999) found that RA prevented phosphorylation of RB in normal human B lymphocytes when these cells were stimulated with anti-m and SAC.…”

Section: Discussionmentioning

confidence: 99%

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Cell cycle genes as targets of retinoid induced ovarian tumor cell growth suppression

et al. 2001

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Cell cycle genes as targets of retinoid induced ovarian tumor cell growth suppression

et al. 2001

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“…Although the past two decades have focused on examining transcriptional mechanisms linked to the pleiotropic effects of RA, the importance of post-translational modification of various proteins has been recently highlighted. RA has been shown to induce ubiquitination of a number of proteins, including cyclin D1 (Spinella et al, 1999), p300 (Brouillard and Cremisi, 2003), and Skp2 (Dow et al, 2001), and IRS-1 is known to be conjugated by ubiquitin (Lee et al, 2000). However, the ubiquitination of IRS-1 by RA has not been reported.…”

Section: Introductionmentioning

confidence: 91%

Retinoic acid mediates degradation of IRS-1 by the ubiquitin–proteasome pathway, via a PKC-dependant mechanism

et al. 2004

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“…NGF requires both increased translation and transcription of cyclin D1 for G 1 entry in early precursors, while BDNF requires only a rapid post-translational mechanism in later precursors. Regulation of cyclin D1 protein levels occurs through a variety of post-translational mechanisms, including alterations in proteolysis, [50][51][52][53][54][55][56] and sequestration. 65 BDNF may act through either mechanism.…”

confidence: 99%

Progressive and Inhibitory Cell Cycle Proteins Act Simultaneously to Regulate Neurotrophin-mediated Proliferation and Maturation of Neuronal Precursors

Simpson

Moon²,

Kleman

et al. 2007

Cell Cycle

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ACKnowlEdGEMEntSWe thank Amy Palmer for helpful discussions and reading of the manuscript, and Susan McTeer for manuscript preparation. This work was supported by grants NIDCD RO3 DC005704 to P.J.S., NIDCD RO1 DC02979 and NINDS RO1 NS39657 to G.V.R. AbStRACtNeuronal stem cell expansion and differentiation is a process involving stages of proliferation and maturation governed by the sequential and combinatorial exposure of cells to extrinsic factors. The olfactory epithelium is an excellent model to investigate regulation of this process, as it undergoes neuronal replacement post-natally. We have shown that the neurotrophins NGF and BDNF sequentially promote proliferation of developing olfactory sensory neuronal precursors, although their kinetics of proliferation and cell fate outcomes differ. Interestingly, CNP inhibits this neurotrophin-induced proliferation and promotes the maturation of these precursors to their next developmental stage. Here, we investigate the mechanisms behind these actions. Both NGF and BDNF increase the expression of cyclin D1 and cyclin-dependent kinase 4 (cdk4), with temporal expression patterns that parallel the proliferation kinetics of their cellular targets. The timing of cyclin D1 expression reflects differences in the need for transcription and translation in early and late stage precursors. CNP inhibits neurotrophin-induced cyclin D1 expression, and induces the expression of different profiles of inhibitory cell cycle proteins, which are neurotrophin-specific and correlate with the attainment of different maturational cell fates. Inhibition of protein degradation reverses the effects of neurotrophins and CNP on cyclin D1 and inhibitor expression levels, respectively. These results suggest a model for cell cycle regulation that involves the simultaneous expression of progressive and inhibitory cell cycle regulatory proteins in response to both proliferation and differentiation agents, followed by selective degradation of these proteins, providing a mechanism for rapid and exquisite control of the cell cycle.

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Retinoic Acid Promotes Ubiquitination and Proteolysis of Cyclin D1 during Induced Tumor Cell Differentiation

Cited by 148 publications

References 49 publications

Cell cycle genes as targets of retinoid induced ovarian tumor cell growth suppression

Cell cycle genes as targets of retinoid induced ovarian tumor cell growth suppression

Retinoic acid mediates degradation of IRS-1 by the ubiquitin–proteasome pathway, via a PKC-dependant mechanism

Progressive and Inhibitory Cell Cycle Proteins Act Simultaneously to Regulate Neurotrophin-mediated Proliferation and Maturation of Neuronal Precursors

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