Cyclin I: A New Cyclin Encoded by a Gene Isolated from Human Brain

Nakamura, Takeshi; Sanokawa, Reiko; Sasaki, Y.; Ayusawa, Dai; Oishi, Michio; Mori, Nozomu

doi:10.1006/excr.1995.1406

Cited by 81 publications

(85 citation statements)

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“…Cyclin G1 was originally identi®ed as a novel member of the cyclin family with homology to c-src (Tamura et al, 1993), and cyclin G2 was isolated as a homologue of cyclin G1 (Horne et al, 1996;Bates et al, 1996). Cyclin I may also belong to the cyclin G subfamily because of its high sequence homology to cyclin G1 and cyclin G2 (Nakamura et al, 1995;Bates et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Cyclin G1 is involved in G2/M arrest in response to DNA damage and in growth control after damage recovery

et al. 2001

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Cyclin G1 is one of the target genes of the transcription factor p53, and is induced in a p53-dependent manner in response to DNA damage. Although cyclin G1 has been implicated in a range of biological phenomena, its precise function remains unclear. Here we present an analysis of the physiological role of cyclin G1 using mice homozygous for a targeted disruption of the cyclin G1 gene. In order to clarify the role of cyclin G1 in the p53 pathway, downstream events such as apoptosis, cell growth and cell cycle checkpoint control were analysed in thymocytes and embryonic ®broblasts derived from cyclin G1-disrupted mice. No di erence was detected in induction of apoptosis between mouse embryo ®broblasts (MEFs) derived from cyclin G1 +/+ and cyclin G1 7/7 mice. Following irradiation, cyclin G1 7/7 MEFs proliferated more slowly and reached lower cell densities in culture dishes than cyclin G1 +/+ MEFs. Analysis of cell survival showed that cyclin G1 7/7 MEFs were about twice as sensitive as cyclin G1 +/+ MEFs to g radiation or UV radiation. Cyclin G1 7/7 mice were more sensitive to g radiation than wild-type mice. Flow cytometeric analysis revealed that the number of cyclin G1 7/7 MEFs in G2/ M phase after irradiation was reduced by 50% relative to cyclin G1 +/+ MEFs. Our results demonstrate that cyclin G1 plays roles in G2/M arrest, damage recovery and growth promotion after cellular stress. Oncogene (2001) 20, 3290 ± 3300.

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Section: Introductionmentioning

confidence: 99%

Cyclin G1 is involved in G2/M arrest in response to DNA damage and in growth control after damage recovery

et al. 2001

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“…At least nine classes of cyclins and seven CDKs, including G1 cyclins (D1-3, E and A) and their catalytic partners, CDKs (2, 4 and 6), have now been isolated (Sherr, 1993(Sherr, , 1994Nakamura et al, 1995;Weinberg et al, 1995). CDK4 and CDK6 are activated by formation of a complex with D-type cyclins which acts as a growth sensor, phosphorylates, and inactivates pRB, the product of the retinoblastoma tumour suppressor gene (Sherr, 1994).…”

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confidence: 99%

Comparison of deregulated expression of cyclin D1 and cyclin E with that of cyclin-dependent kinase 4 (CDK4) and CDK2 in human oesophageal squamous cell carcinoma

Matsumoto

Furihata

Ishikawa³

et al. 1999

Br J Cancer

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SummaryThe expressions of cyclin D1, cyclin E, cyclin-dependent kinase 4 (CDK4), and CDK2 were immunohistochemically examined in 90 patients with human oesophageal squamous cell carcinoma (SCC) to determine their relationship to the tumour behaviour and patient prognosis. Nuclear immunostaining of cyclin D1 and cyclin E was observed in 28 (31.1%) and 27 tumours (30.0%) respectively. Thirty-nine tumours (43.3%) and 31 tumours (34.4%) exhibited both cytoplasmic and nuclear positivity for CDK4 and CDK2 respectively. Of 28 cyclin D1-positive and 27 cyclin E-positive tumours, CDK4 was overexpressed in 12 (42.8%) tumours and CDK2 in seven (25.9%) tumours respectively. There was no significant relationship in immunopositivity between cyclin D1 and CDK4 or between cyclin E and CDK2. Simultaneous immunoreactivity for both cyclin D1 and CDK4 was significantly associated with venous invasion (P < 0.05). In a univariate analysis, the prognosis of patients with tumours that were both cyclin D1-and CDK4-positive was significantly poorer than that of patients with cyclin D1-negative tumours (P < 0.05). In a multivariate analysis, both cyclin D1 and CDK4 immunoreactivities (P < 0.01) and tumour stage (P < 0.001) were recognized as independent risk factors. In this analysis, the hazard ratio for cyclin D1-positive and CDK4-negative cases compared with cyclin D1-negative cases was significant (hazard ratio = 3.128, 95% confidence interval = 1.418-6.899, P = 0.0047). No significant prognostic relevance was detected in both cyclin E and CDK2 immunoreactivity. Our in vivo findings suggest that in human oesophageal SCC, cyclin D1 and cyclin E and their functional partners, CDK4 and CDK2, often exhibit dysregulated overexpression in many cases, and that tumours with simultaneous expression of cyclin D1 and CDK4 are frequently associated with venous invasion and have a worse prognosis, statistically. Moreover, overexpression of cyclin D1 alone may also contribute to tumour progression independent of CDK4 overexpression.

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“…Although the clinical importance of AHRdependent activation of CCNG2 remains to be investigated, trastuzumab treatment has also been reported to increase CCNG2 levels (22). RNAi-mediated knockdown of CCNG2 resulted in a slight reduction in trastuzumabdependent growth inhibition, suggesting that CCNG2 is required, but not necessary, for the inhibitory action of trastuzumab (18,40). However, the mechanism of CCNG2 upregulation by trastuzumab most likely does not require FOXA1, as it is not expressed in ER-negative breast cancer (41).…”

Section: Discussionmentioning

confidence: 99%

FOXA1 Is Essential for Aryl Hydrocarbon Receptor–Dependent Regulation of Cyclin G2

Ahmed

Al-Saigh

Matthews

2012

Molecular Cancer Research

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The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the effects of the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Recently, AHR has emerged as a potential therapeutic target for breast cancer by virtue of its ability to modulate estrogen receptor-a (ERa) signalling and/or its ability to block cell proliferation. Our previous studies identified cyclin G2 (CCNG2), an inhibitor of cellcycle progression, as an AHR target gene; however, the mechanism of this regulation is unknown. Chromatin immunoprecipitation assays in T-47D human breast cancer cells revealed a TCDD-dependent recruitment of AHR, nuclear co-activator 3 (NCoA3) and the transcription factor forkhead box A1 (FOXA1), a key regulator of breast cancer cell signaling, to CCNG2 resulting in increases in CCNG2 mRNA and protein levels. Mutation of the AHR response element (AHRE) and forkhead-binding sites abolished TCDD-induced CCNG2-regulated reporter gene activity. RNA interference-mediated knockdown of FOXA1 prevented the TCDD-dependent recruitment of AHR and NCoA3 to CCNG2 and reduced CCNG2 mRNA levels. Interestingly, knockdown of FOXA1 also caused a marked decrease in ERa, but not AHR protein levels. However, RNA interference-mediated knockdown of ERa, a negative regulator of CCNG2, had no effect on TCDD-dependent AHR or NCoA3 recruitment to or expression of CCNG2. These findings show that FOXA1, but not ERa, is essential for AHR-dependent regulation of CCNG2, assigning a role for FOXA1 in AHR action. Mol Cancer Res; 10(5); 636-48. Ó2012 AACR.

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Cyclin I: A New Cyclin Encoded by a Gene Isolated from Human Brain

Cited by 81 publications

References 0 publications

Cyclin G1 is involved in G2/M arrest in response to DNA damage and in growth control after damage recovery

Cyclin G1 is involved in G2/M arrest in response to DNA damage and in growth control after damage recovery

Comparison of deregulated expression of cyclin D1 and cyclin E with that of cyclin-dependent kinase 4 (CDK4) and CDK2 in human oesophageal squamous cell carcinoma

FOXA1 Is Essential for Aryl Hydrocarbon Receptor–Dependent Regulation of Cyclin G2

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