The effect of cyclin D expression on cell proliferation in human gliomas

Zhang, Xiang; Zhao, Ming; Anyang, Huang; Zhou, Fengjiao; Zhang, Wei; Wang, Xiling

doi:10.1016/j.jocn.2004.03.036

Cited by 47 publications

(34 citation statements)

References 11 publications

(13 reference statements)

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“…Cyclin D1 is well established as an oncogene with an important pathogenetic role in several human tumors (Fu et al 2004;Arnold and Papanikolaou 2005). Several studies investigating astrocytic tumors showed increased cyclin D1 expression that correlated with histological grade (Chakrabarty et al 1996;Cavalla et al 1998;Zhang et al 2005). In our study, the cyclin D1 LI was higher in glioblastoma than in diffuse astrocytomas, but the differences did not reach statistical significance, probably because of the low number of diffuse astrocytomas within this series.…”

Section: Discussioncontrasting

confidence: 83%

Eukaryotic Initiation Factors (eIF) 2α and 4E Expression, Localization, and Phosphorylation in Brain Tumors

Tejada

Lobo

García-Villanueva

et al. 2009

J Histochem Cytochem.

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(MVTL) S U M M A R Y Increased protein synthesis is regulated, in part, by two eukaryotic translation initiation factors (eIFs): eIF4E and eIF2a. One or both of these factors are often overexpressed in several types of cancer cells; however, no data are available at present regarding eIF4E and eIF2a levels in brain tumors. In this study, we analyzed the expression, subcellular localization and phosphorylation states of eIF4E and eIF2a in 64 brain tumors (26 meningiomas, 16 oligodendroglial tumors, and 22 astrocytomas) and investigated the correlation with the expression of MIB-1, p53, and cyclin D1 proteins as well. There are significant differences in the phosphorylated eIF4E levels between the tumors studied, being the highest in meningiomas and the lowest in the oligodendroglial tumors. Relative to subcellular localization, eIF4E is frequently found in the nucleus of the oligodendroglial tumors and rarely in the same compartment of the meningiomas, whereas eIF2a showed an inverse pattern. Finally, cyclin D1 levels directly correlate with the phosphorylation status of both factors. The different expression, phosphorylation, or/and subcellular distribution of eIF2a and eIF4E within the brain types of tumors studied could indicate that different pathways are activated for promoting cell cycle proliferation, for instance, leading to increased cyclin D1 expression. (J Histochem Cytochem 57:503-512, 2009)

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Section: Discussioncontrasting

confidence: 83%

Eukaryotic Initiation Factors (eIF) 2α and 4E Expression, Localization, and Phosphorylation in Brain Tumors

Tejada

Lobo

García-Villanueva

et al. 2009

J Histochem Cytochem.

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“…We also observed that the increase in the temozolomide-induced apoptosis in all of these cells was associated with a methylation of the survivin and bcl-w genes, both of which encoded for antiapoptotic proteins. The choice of these genes was supported by the fact that survivin and Bcl-w overexpressions are associated with a poor prognosis in glioma patients and with highly invasive gliomas, respectively (29)(30)(31), and the survivin gene was frequently unmethylated in glioma (32). In parallel to this, we investigated whether the decrease in proliferation observed with a folate supplementation was associated with a methylation of the PDGF-B gene because the expression of this growth factor is epigenetically regulated in gliomas (15), and the PDGF-B acts as an oncogenic factor in gliomagenesis (25,33).…”

Section: Resultsmentioning

confidence: 99%

Folate Supplementation Limits the Aggressiveness of Glioma via the Remethylation of DNA Repeats Element and Genes Governing Apoptosis and Proliferation

Hervouet

Debien

Campion

et al. 2009

Clinical Cancer Research

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Purpose: We have investigated whether the folate supplementation could be used to limit the aggressiveness of glioma through the DNA remethylation because (a) the cancer genome is characterized by a low level of DNA methylation (or 5-methylcytosine, 5 mC); and (b) folate is the main generator of S-adenosyl-methionine, the methyl donor molecule in the DNA methylation reaction catalyzed by the DNA methyltranferases. Experimental Design: The effects of folate supplementations were analyzed on the global DNA methylation status, the methylation status of DNA repeat element, the sensitivity of temozolomide-induced apoptosis, and the proliferation index of glioma cells. Finally, we analyzed whether the DNA methylation level could be used as a prognostic factor and/or a biomarker in an antiglioma therapy using folate supplementation as an adjuvant. Results: Our data show that gliomagenesis is accompanied by a reduction in 5 mC levels and that this low level of 5 mC is a poor prognostic factor in Glioblastoma Multiforme patients. We also show that folate supplementation enhanced the DNA remethylation through the Sp1/Sp3-mediated transcriptional up-regulation of genes coding for Dnmt3a and Dnmt3b proteins, two de novo methyltranferases. Finally, we show that the folate-induced DNA methylation limits proliferation and increases the sensitivity to temozolomide-induced apoptosis in glioma cells through methylation of the genes implicated in these processes (PDGF-B, MGMT, survivin, and bcl-w). Conclusion: This study suggests that folate supplementation could be a promising adjuvant for the future design of antiglioma therapies in preclinical and/or clinical studies.Despite the irrefutable role of genetic mechanisms in triggering tumorigenesis, epigenetic modifications, and particularly the DNA methylation modifications, are now recognized as frequent alterations playing a crucial role in the development and progression of human malignancies (1-3). Two distinct DNA methylation abnormalities are observed in cancer. The first is an overall genome-wide reduction in DNA methylation (global hypomethylation) and the second is regional hypomethylation or hypermethylation within the CpG islands of specific gene promoters. Both forms of hypomethylation are believed to induce proto-oncogene activation and chromosomal instability, whereas regional hypermethylation is strongly associated with transcriptional silencing of tumor suppressor genes (4). Thus, DNA methylation can function as a "switch" to activate or repress gene transcription, providing an important mechanism for overexpressed or silenced genes involved in the regulation of the cell cycle, DNA repair, growth signaling, angiogenesis, and apoptosis, and by ricochet in the initiation and the development of tumors (5).To date, an increasing number of reports investigating epigenetic signatures in malignant gliomas and more particularly the hypermethylation of tumor suppressor genes have been published. For example, it has been reported that PTEN methylation occurs frequen...

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“…25,26 The androgen receptor (AR) is known to play a critical role in prostate cancer progression. Therefore, depletion of AR function (either through androgen ablation or AR antagonist) is the first line of therapeutic treatment for prostate cancer.…”

Section: Discussionmentioning

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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(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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The effect of cyclin D expression on cell proliferation in human gliomas

Cited by 47 publications

References 11 publications

Eukaryotic Initiation Factors (eIF) 2α and 4E Expression, Localization, and Phosphorylation in Brain Tumors

Eukaryotic Initiation Factors (eIF) 2α and 4E Expression, Localization, and Phosphorylation in Brain Tumors

Folate Supplementation Limits the Aggressiveness of Glioma via the Remethylation of DNA Repeats Element and Genes Governing Apoptosis and Proliferation

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

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