Tissue-Specific Consequences of Cyclin D1 Overexpression in Prostate Cancer Progression

He, Yang; Franco, Omar E.; Jiang, Ming; Williams, Karin; Love, Harold D.; Coleman, Ilsa M.; Nelson, Peter S.; Hayward, Simon W.

doi:10.1158/0008-5472.can-07-0418

Cited by 62 publications

(66 citation statements)

References 47 publications

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“…It plays an essential role in the development and progression of several cancers including breast, esophagus, bladder, and lung cancer (Lin et al 2000, Musgrove 2006, He et al 2007. Our results showed that in MCF-7 cells, a high-glucose condition led to decreased expression of cyclin D1 compared with a normal-glucose condition (Fig.…”

Section: Alteration In Expression Of Cyclin D1 By High Glucose and Inmentioning

confidence: 51%

High glucose and insulin differentially modulates proliferation in MCF-7 and MDA-MB-231 cells

Gupta

Tikoo

2013

Journal of Molecular Endocrinology

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Various preclinical and clinical studies have linked diabetes and breast cancer, but little is known regarding the molecular mechanism involved. This study aimed to investigate the effect of high glucose and insulin in breast cancer cells (MCF-7: non-invasive, hormone dependent, and MDA-MB-231: invasive, hormone independent). In contrast to MCF-7 cells, high glucose augmented proliferation of MDA-MB-231 cells as observed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and bromodeoxyuridine assays. The high-glucose condition led to increased expression of cyclin D1, de-phosphorylation of p38, and increased phosphorylation of ERK in MDA-MB-231 cells but not in MCF-7 cells. Interestingly, we observed increased phosphorylation of GSK-3b, NF-kB, and ERa only in MCF-7 cells, highlighting their role as potential targets in prevention of progression of breast cancer under a high-glucose and insulin condition. Furthermore, insulin treatment under a high-glucose condition resulted in increased histone H3 phosphorylation and de-acetylation only in MDA-MB-231 cells. Taken together, we provide the first evidence that high glucose and insulin promotes proliferation of MDA-MB-231 cells by differential alteration of GSK-3b, NF-kB, and ERa expression and histone H3 modifications, which may directly or indirectly modulate the expression of genes involved in its proliferation.

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Section: Alteration In Expression Of Cyclin D1 By High Glucose and Inmentioning

confidence: 51%

High glucose and insulin differentially modulates proliferation in MCF-7 and MDA-MB-231 cells

Gupta

Tikoo

2013

Journal of Molecular Endocrinology

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“…Similarly, SENP1 moderates the expression of the cell cycle regulator, cyclin D1; diminishing SENP1 in PCa cells decreases cyclin D1 levels (18). Previous studies indicate that enhanced expression of cyclin D1 is readily observed in advanced PCa (19,20) and contributes to PCa pro-gression (21,22). Therefore, the expression of SENP1 in PCa cells modulates major factors in PCa progression.…”

mentioning

confidence: 95%

Induction of the SUMO-specific Protease 1 Transcription by the Androgen Receptor in Prostate Cancer Cells

Bawa-Khalfe

Cheng

Wang

et al. 2007

Journal of Biological Chemistry

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Prostate cancer, the most frequently diagnosed carcinoma in males, is readily modulated via the transcriptional activity of androgen receptors. Our recent publication reported that androgen receptor-dependent transcription is significantly elevated with expression of the human sentrin/SUMO-specific protease (SENP1) in the androgen-sensitive human prostate cancer cell line (LNCaP). In situ hybridization studies indicated an elevation of SENP1 message in prostatic intraepithelial neoplasia and prostate cancer lesions as compared with normal prostate epithelia. This study aimed to delineate the mechanism for the regulation of SENP1 message and to determine the pathophysiological consequence of SENP1 induction with respect to prostate cancer. Real-time PCR confirmed the elevation of SENP1 mRNA in prostate cancer cells as compared with normal prostate epithelial cells. Chronic androgen exposure of LNCaP cells prompted an enhancement in the SENP1 transcript selectively. This androgen-mediated augmentation of SENP1 was absent with co-administration of the androgen receptor antagonist bicalutamide and in androgen receptor-negative prostate cancer PC-3 cells, indicating an androgen receptor-dependent event. Activation of the androgen receptor was required for binding an identified androgen response element and positively regulating SENP1 promoter activity. Abrogation of elevated SENP1 mRNA in prostate cancer cells significantly decreased androgen-mediated cell growth. Because increased SENP1 expression directly modulated androgen receptor-dependent cell proliferation and transcription, SENP1 could play an important role in prostate carcinogenesis. Small ubiquitin-like modifier (SUMO)3 mediates a diverse array of cellular events by conjugating to numerous protein substrates. Recent reports have focused on the ability of SUMOylation to regulate the transcriptional activity of nuclear receptors, transcription factors, and co-regulatory proteins (1-6). The three mammalian SUMO proteins, SUMO1, SUMO2, and SUMO3, form covalent bonds with cellular targets in a sequential manner analogous to ubiquitin (7,8). A family of human SUMO-specific proteases (SENP) (9) can selectively deconjugate SUMOylated proteins and hence dictate SUMO dynamics. Our laboratory cloned the first human SUMO protease, SENP1 (9), and since its discovery, SENP1 has become the best characterized of the SENP family. It is localized exclusively in the nucleus and deconjugates many SUMO substrates (9 -11). SENP1 shares the greatest homology with SENP2 (9, 12, 13). In contrast, SENP1 differs significantly from SENP3 and SENP5, which constitute an independent subfamily based on their nucleolar localization and preference for deSUMOylation of SUMO2 and SUMO3 conjugates (14).Recently, we reported that SENP1 plays a prominent role in the regulation of the androgen receptor (AR)-dependent transcription (10). Under physiological conditions, the AR dictates the development and normal growth of the prostate gland. The androgen 5␣-dihydrotestosterone binds AR to prompt t...

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“…There was no significant difference of p53 expression between the groups (LI: 11.86 ± 19.51 and 2.03 ± 2.27, respectively; p > 0.05) (Figures 1F1, F2). For most tumors (27/43), the expression intensity was weak or moderate (2)(3)(4)(5)(6)). An intense expression (9) was observed in three cases and it comprised over 60% of cancer cells.…”

Section: Statisticsmentioning

confidence: 99%

“…The proliferation rate, a feature that has been proven to be an unfavorable prognostic factor in many cancers, was evaluated using its two widely known indicators: Ki-67 (Mib-1) protein, which is expressed by proliferating cells during all active phases of the cell cycle, and cyclin D1, which is involved in controlling the G1/S phase [1][2][3].…”

mentioning

confidence: 99%

“…CD44 glycoprotein performs the function of a cellular surface receptor for hyaluronic acid, a glycoaminoglycoside which takes part in cancer cell metastasizing [12]. Three forms of CD44 have been identified: full length (exons [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20], standard (exons [1][2][3][4][5][16][17][18][19][20] and CD44v [13].…”

mentioning

confidence: 99%

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Comparative analysis of biological profiles of benign prostate hyperplasia and prostate cancer as potential diagnostic, prognostic and predictive indicators

Makarewicz¹,

Żyromska²,

Andrusewicz³

2011

Folia Histochem Cytobiol.

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Tissue-Specific Consequences of Cyclin D1 Overexpression in Prostate Cancer Progression

Cited by 62 publications

References 47 publications

High glucose and insulin differentially modulates proliferation in MCF-7 and MDA-MB-231 cells

High glucose and insulin differentially modulates proliferation in MCF-7 and MDA-MB-231 cells

Induction of the SUMO-specific Protease 1 Transcription by the Androgen Receptor in Prostate Cancer Cells

Comparative analysis of biological profiles of benign prostate hyperplasia and prostate cancer as potential diagnostic, prognostic and predictive indicators

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