Regulation of cyclin D1 gene expression

Witzel, Ini Isabée; Koh, Li Fang; Perkins, Neil D.

doi:10.1042/bst0380217

Cited by 108 publications

(92 citation statements)

References 48 publications

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“…NF-κB also exhibits a central role in the proliferating airway epithelium of asthmatics (36). Its interplay with different cell cycle control genes including TP53 and CCND1 is diverse (37,38). Compatible with this picture, leptin and adiponectin have also been found to be able to modulate expression levels of cyclin D1 or p53 in different types of cancer cells (39,40).…”

Section: Ccnd1 Modifies the Asthma-obesity Association 151mentioning

confidence: 89%

The Association of a Variant in the Cell Cycle Control GeneCCND1and Obesity on the Development of Asthma in the Swiss SAPALDIA Study

Thun¹,

Imboden²,

Berger³

et al. 2013

Journal of Asthma

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OBJECTIVE: The molecular mechanisms underlying the association between obesity (BMI 30 kg/m(2)) and asthma are poorly understood. Since shifts in the fate of bronchial cells due to lowgrade systemic inflammation may provide a possible explanation, we investigated whether two of the best documented functional variants in cell cycle control genes modify the obesity-asthma association. METHODS: We genotyped 5930 SAPALDIA cohort participants for the single-nucleotide polymorphisms (SNPs) rs9344 in the cyclin D1 gene (CCND1) and rs1042522 in the gene encoding tumor protein 53 (TP53). We assessed the independent association of these SNPs and obesity with asthma prevalence and incidence. RESULTS: The CCND1 SNP modified the association between obesity and asthma prevalence (p(interaction )= 0.03). The odds ratios (ORs) and 95% confidence intervals (CIs) for reporting a physician diagnosis of asthma at baseline, comparing obese with non-obese participants, were 1.09 (0.51-2.33), 1.64 (0.94-2.88), and 3.51 (1.63-7.53) for GG, GA, and AA genotypes, respectively. We found comparable genotype differences for incident asthma within the 11 years of follow-up. As for the TP53 SNP, the interactions with obesity status with respect to asthma were not statistically significant. CONCLUSIONS: Our results suggest that obesity may contribute to asthma and associated tissue remodeling by modifying the processes related to the CCND1 gene activity. Objective. The molecular mechanisms underlying the association between obesity (BMI 30 kg/m 2 ) and asthma are poorly understood. Since shifts in the fate of bronchial cells due to low-grade systemic inflammation may provide a possible explanation, we investigated whether two of the best documented functional variants in cell cycle control genes modify the obesity-asthma association. Methods. We genotyped 5930 SAPALDIA cohort participants for the single-nucleotide polymorphisms (SNPs) rs9344 in the cyclin D1 gene (CCND1) and rs1042522 in the gene encoding tumor protein 53 (TP53). We assessed the independent association of these SNPs and obesity with asthma prevalence and incidence. Results. The CCND1 SNP modified the association between obesity and asthma prevalence (p interaction ¼ 0.03). The odds ratios (ORs) and 95% confidence intervals (CIs) for reporting a physician diagnosis of asthma at baseline, comparing obese with non-obese participants, were 1.09 (0.51-2.33), 1.64 (0.94-2.88), and 3.51 (1.63-7.53) for GG, GA, and AA genotypes, respectively. We found comparable genotype differences for incident asthma within the 11 years of follow-up. As for the TP53 SNP, the interactions with obesity status with respect to asthma were not statistically significant. Conclusions. Our results suggest that obesity may contribute to asthma and associated tissue remodeling by modifying the processes related to the CCND1 gene activity.of Asthma, 2013; 50(2): 147-154 Copyright © 2013 Informa Healthcare USA, Inc. ISSN: 0277-0903 print/1532-4303

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Section: Ccnd1 Modifies the Asthma-obesity Association 151mentioning

confidence: 89%

The Association of a Variant in the Cell Cycle Control GeneCCND1and Obesity on the Development of Asthma in the Swiss SAPALDIA Study

Thun¹,

Imboden²,

Berger³

et al. 2013

Journal of Asthma

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“…Given its important role in cell cycle, the expression of CCND1 needs to be strictly ruled. It is subject to all aspects of regulation, including gene transcription, RNA processing, splicing, modification, protein stability and cellular localization (Witzel et al, 2010). Deregulation of any of these procedures could induce overexpression of CCND1, and subsequently promote tumorigenesis in many kinds of cells (Fu et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-576-3p Inhibits Proliferation in Bladder Cancer Cells by Targeting Cyclin D1

Liang¹,

Li²,

Xu³

et al. 2015

Molecules and Cells

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MicroRNAs (miRNAs) are small, endogenous RNAs that play important gene-regulatory roles by binding to the imperfectly complementary sequences at the 3-UTR of mRNAs and directing their gene expression. Here, we first discovered that miR-576-3p was down-regulated in human bladder cancer cell lines compared with the non-malignant cell line. To better characterize the role of miR-576-3p in bladder cancer cells, we over-expressed or down-regulated miR-576-3p in bladder cancer cells by transfecting with chemically synthesized mimic or inhibitor. The overexpression of miR-576-3p remarkably inhibited cell proliferation via G1-phase arrest, and decreased both mRNA and protein levels of cyclin D1 which played a key role in G1/S phase transition. The knock-down of miR-576-3p significantly promoted the proliferation of bladder cancer cells by accelerating the progression of cell cycle and increased the expression of cyclin D1. Moreover, the dual-luciferase reporter assays indicated that miR-576-3p could directly target cyclin D1 through binding its 3-UTR. All the results demonstrated that miR-576-3p might be a novel suppressor of bladder cancer cell proliferation through targeting cyclin D1.

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“…Because cyclin D1 plays a permissive role in cell cycle progression, it is not surprising that cells employ multiple mechanisms in its regulation in response to a plethora of stimuli (14,15,18,34). However, what is not known is whether there is any cross-talk among the multiple transcription factors that are activated by various signaling mechanisms in the induction of cyclin D1 expression in mediating cell cycle progression and cell migration in response to an agonist.…”

mentioning

confidence: 98%

Novel Interactions between NFATc1 (Nuclear Factor of Activated T Cells c1) and STAT-3 (Signal Transducer and Activator of Transcription-3) Mediate G Protein-coupled Receptor Agonist, Thrombin-induced Biphasic Expression of Cyclin D1, with First Phase Influencing Cell Migration and Second Phase Directing Cell Proliferation

Kundumani‐Sridharan

Quyền

Singh

et al. 2012

Journal of Biological Chemistry

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Background: NFATc1 and STAT-3 associate with each other constitutively and regulate cyclin D1 expression in response to thrombin, a G protein-coupled receptor agonist. Results: NFATc1 exists in complex with STAT-3 and modulates its acetylation via recruiting p300 in the biphasic expression of cyclin D1 facilitating VSMC migration and proliferation. Conclusion: NFATc1-STAT-3 cooperatively binds to cyclin D1 promoter and modulates its activity. Significance: NFATc1-STAT-3 interactions may play a role in vascular diseases and cancer.

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Regulation of cyclin D1 gene expression

Cited by 108 publications

References 48 publications

The Association of a Variant in the Cell Cycle Control GeneCCND1and Obesity on the Development of Asthma in the Swiss SAPALDIA Study

The Association of a Variant in the Cell Cycle Control GeneCCND1and Obesity on the Development of Asthma in the Swiss SAPALDIA Study

MicroRNA-576-3p Inhibits Proliferation in Bladder Cancer Cells by Targeting Cyclin D1

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