The cyclin D1 proto-oncogene is sequestered in the cytoplasm of mammalian cancer cell lines

Alao, John P.; Gamble, Simon C.; Stavropoulou, Alexandra; Pomeranz, Karen M.; Lam, Eric W.‐F.; Coombes, R. Charles; Vigushin, David M.

doi:10.1186/1476-4598-5-7

Cited by 61 publications

(33 citation statements)

References 23 publications

(38 reference statements)

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“…At the end point, the average volume of the tumors expressing WWOX and of the control plasmid were 390 § 115 and 890 § 170 mm 3 , respectively (p < 0.001, two-way ANOVA). In addition, the average volume of the WWOX-silenced tumors was 1190 § 240 mm 3 , which was slightly bigger than the control group (890 § 170 mm 3 ). Taken together, WWOX suppressed cell proliferation in vitro and tumor growth in vivo, suggesting that WWOX acts as a tumor suppressor in prostate cancer.…”

Section: Wwox Repressed Prostate Tumor Progression In Vivo and In Vitromentioning

confidence: 99%

“…2 The cyclin D1 proto-oncogene is an important regulator of G1 to S phase transition, and its overexpression is commonly found in cancers including prostate cancer. 3 Dysregulation of cyclin D1 has been reported to contribute to an increase not only in tumor cell growth but also in chromosome instability. 4 These alterations may further contribute to tumor progression and the acquisition of an aggressive phenotype.…”

Section: Introductionmentioning

confidence: 99%

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WWOX suppresses prostate cancer cell progression through cyclin D1-mediated cell cycle arrest in the G1 phase

Lin

Chang

et al. 2015

Cell Cycle

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(2015) WWOX suppresses prostate cancer cell progression through cyclin D1-mediated cell cycle arrest in the G1 phase, Cell Cycle, 14:3, 408-416, DOI: 10.4161/15384101.2014 WW domain-containing oxidoreductase (WWOX) has been reported to be a tumor suppressor in multiple cancers, including prostate cancer. WWOX can induce apoptotic responses to inhibit tumor progression, and the other mechanisms of WWOX in tumor suppression have also been reported recently. In this study, we found significant down-regulation of WWOX in prostate cancer specimens and prostate cancer cell lines compared with the normal controls. In addition, an ectopically increased WWOX expression repressed tumor progression both in vitro and in vivo. Interestingly, overexpression of WWOX in 22Rv1 cells led to cell cycle arrest in the G1 phase but did not affect sub-G1 in flow cytometry. GFP-WWOX overexpressed 22Rv1 cells were shown to inhibit cell cycle progression into mitosis under nocodazole treatment in flow cytometry, immunoblotting and GFP fluorescence. Further, cyclin D1 but not apoptosis correlated genes were down-regulated by WWOX both in vitro and in vivo. Restoration of cyclin D1 in the WWOXoverexpressed 22Rv1 cells could abolish the WWOX-mediated tumor repression. In addition, WWOX impair c-Junmediated cyclin D1 promoter activity. These results suggest that WWOX inhibits prostate cancer progression through negatively regulating cyclin D1 in cell cycle lead to G1 arrest. In summary, our data reveal a novel mechanism of WWOX in tumor suppression.

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Section: Wwox Repressed Prostate Tumor Progression In Vivo and In Vitromentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

WWOX suppresses prostate cancer cell progression through cyclin D1-mediated cell cycle arrest in the G1 phase

Lin

Chang

et al. 2015

Cell Cycle

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“…mAChR subtypes are widely expressed in the central and peripheral nervous systems [4,28]. Previous different studies postulated that muscarinic acetylcholine receptors are functional in some hematopoietic cells [8,[21][22][23][24][25][26][27][28][29]. Our previous RT-PCR studies have shown that M 2 , M 3 and M 4 mAChR subtypes are expressed in K562 cells and suggested that they are involved in regulation of NO signaling and adenylate cyclase activity [8,29].…”

Section: Discussionmentioning

confidence: 99%

“…Different studies showed that cyclin D 1 is a predominantly cytoplasmic protein in mammalian cancer cell lines [23]. The aim of this study was to examine muscarinic receptor mediated c-Fos and cyclin D 1 gene expression in K562 cells and to investigate the intracellular signaling pathways that couple receptor stimulation to these genes.…”

Section: +mentioning

confidence: 99%

Muscarinic Agonist, Antagonists and Signaling Pathway Inhibitors Change c-Fos And Cyclin D1 Expression in K562 Cells

Cabadak¹,

Aydın²,

Kan³

2013

MMJ

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Acetylcholine is a neurotransmitter in the nervous system but it serves also as a paracrine or autocrine factor in different cell types, where it is linked to functions like proliferation and cell differentiation [1][2][3]. mAChRs mediate a wide array of cellular responses to acetylcholine in the central nervous system (CNS) and in non-nervous tissues innervated by the parasymphatic nervous system [4,5]. Muscarinic receptors are involved in diverse actions, including inhibition of adenylate cyclase, breakdown of phosphoinositide, regulation of nitric oxide (NO) synthesis, change of Ca 2+ levels and modulation of K channels [6][7][8]. Muscarinic cholinergic receptors can also induce cell proliferation, differentiation and transformation. These effects are cell type dependent and receptor subtype specific. Many cells express a mixture of muscarinic receptor

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“…Besides gene amplification, cytoplasmic sequestration may also serve to regulate cyclin D1 activity in mammalian cancer cells [26]. Emerging evidence indicates that cyclin D1 may act, in part, through pathways which do not involve its role as a cell cycle regulator.…”

Section: Cyclin D and Cancermentioning

confidence: 99%

Cell cyclins: triggering elements of cancer or not?

et al. 2010

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Cyclins are indispensable elements of the cell cycle and derangement of their function can lead to cancer formation. Recent studies have also revealed more mechanisms through which cyclins can express their oncogenic potential. This review focuses on the aberrant expression of G1/S cyclins and especially cyclin D and cyclin E; the pathways through which they lead to tumour formation and their involvement in different types of cancer. These elements indicate the mechanisms that could act as targets for cancer therapy.

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The cyclin D1 proto-oncogene is sequestered in the cytoplasm of mammalian cancer cell lines

Cited by 61 publications

References 23 publications

WWOX suppresses prostate cancer cell progression through cyclin D1-mediated cell cycle arrest in the G1 phase

WWOX suppresses prostate cancer cell progression through cyclin D1-mediated cell cycle arrest in the G1 phase

Muscarinic Agonist, Antagonists and Signaling Pathway Inhibitors Change c-Fos And Cyclin D1 Expression in K562 Cells

Cell cyclins: triggering elements of cancer or not?

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