Molecular cloning and chromosomal mapping of CCND genes encoding human D-type cyclins

Xiong, Yue; Menninger, Joan C.; Beach, David; Ward, David C.

doi:10.1016/0888-7543(92)90127-e

Cited by 178 publications

(101 citation statements)

References 29 publications

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“…Mice lacking cyclin Ds die in mid/late gestation, and cells without cyclin Ds exhibit reduced susceptibility to oncogenic transformation (Kozar et al, 2004). In mammalian cells there are three types of cyclin Ds, D1, D2 and D3 (Xiong et al, 1992). There is functional redundancy among these cyclin Ds, as it has been shown that cyclin D2 could substitute the function of cyclin D1 in mouse development (Carthon et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

GSK3β mediates suppression of cyclin D2 expression by tumor suppressor PTEN

Huang

et al. 2006

Oncogene

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PTEN, encoding a lipid phosphatase, is a tumor suppressor gene and is mutated in various types of cancers. It is reported to regulate G1 to S phase transition of the cell cycle by influencing the expression, protein stability and subcellular location of cyclin D1. Here, we provide evidence that PTEN modulates the transcription and protein stability of cyclin D2. Targeted deletion of Pten in mouse embryonic fibroblasts (MEFs) endowed cells with greater potential to overcome G1 arrest than wild-type MEFs and led to the elevated expression of cyclin D2, which was suppressed by the introduction of PTEN. We further defined a pathway involving GSK3b and b-catenin/TCF in PTEN-mediated suppression of cyclin D2 transcription. LiCl, an inhibitor of GSK3b, abolished inhibitory effect of PTEN on cyclin D2 expression, and TCF members could directly bind to the promoter of cyclin D2 and regulate its transcription in a CREB-dependent manner. Our results indicate that the downregulation of cyclin D2 expression by PTEN is mediated by the GSK3b/b-catenin/TCF pathway in cooperation with CREB, and suggest a convergence from the PI-3 kinase/PTEN pathway and the Wnt pathway in modulation of cyclin D2 expression.

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Section: Introductionmentioning

confidence: 99%

GSK3β mediates suppression of cyclin D2 expression by tumor suppressor PTEN

Huang

et al. 2006

Oncogene

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“…Cyclin D1 is a 36-Kda protein that belongs to a family of cell-cycle regulators called cyclins (Xiong et al, 1991(Xiong et al, , 1992a. It functions in the G1 phase of cell cycle and activates the kinase activities of G1 cyclindependent kinases (for review, see Sherr, 1993Sherr, , 1994.…”

Section: Introductionmentioning

confidence: 99%

Increased cell growth and tumorigenicity in human prostate LNCaP cells by overexpression to cyclin D1

et al. 1998

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Deregulated expression of cyclin D1 has been found in several types of human tumors. In order to investigate factors involved in human prostate cancer progression, we studied the e ects of cyclin D1 overexpression on human prostate cancer cell proliferation and tumorigenicity by transfecting LNCaP cells with a retroviral vector containing human cyclin D1 cDNA. When compared to the parental and control-vector transfected LNCaP cells, these cyclin D1-transfected cells had more cells in Sphase and lower growth factor requirements. Furthermore, these cells grew more in androgen-free medium. We also detected higher levels of Rb phosphorylation and E2F-1 protein levels in LNCaP/cyclin D1 cells than that in the parental and vector control cells in medium with or without androgen. Cyclin D1 transfected clones formed tumors more rapidly than control and parental cells. These tumors were refractory to the androgen-ablation treatment by castration, whereas tumors from parental and vector-control LNCaP cells regressed within 4 weeks after castration. These results suggest that overexpression of cyclin D1 changes the growth properties, increases tumorigenicity and decreases the requirement for androgen stimulation in LNCaP cells both in vitro and in vivo.

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“…1 Gene copy number increase is an important mechanism leading to abnormal expression of known oncogenes such as MYC at 8q24, CCND1 at 11q13, or HER2 at 17q21. [2][3][4] However, most of the chromosomal regions found amplified in bladder cancer 1 do not contain known oncogenes, suggesting that many amplification target genes remain to be identified.…”

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confidence: 99%

TRIO Amplification and Abundant mRNA Expression Is Associated with Invasive Tumor Growth and Rapid Tumor Cell Proliferation in Urinary Bladder Cancer

Zheng

Simon

Mirlacher

et al. 2004

The American Journal of Pathology

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Studies by comparative genome hybridization have suggested that 5p amplification is related to tumor progression in urinary bladder cancer. In this study seven genes (TAS2R, ADCY2, DNAH5, CTNND2, TRIO, ANKH, and MYO10) located to 5p15.31-5p15.1 were analyzed by fluorescence in situ hybridization using a tissue microarray containing samples from tumors and cell lines with known 5p amplification by comparative genome hybridization. Amplification frequency was highest for TRIO, which maps to 5p15.2 and encodes a protein with a putative role in cellcycle regulation. To further investigate the role of TRIO amplification in bladder cancer, a tissue microarray containing samples from 2317 bladder tumors was used for fluorescence in situ hybridization analysis. TRIO amplification was strongly associated with invasive tumor phenotype, high tumor grade, and rapid tumor cell proliferation (Ki67 LI) (P < 0.0001 each). Only 7 of 456 pTaG1/G2 tumors (1.5%) but 62 of 485 pT1-4 carcinomas (12.8%) had TRIO amplification. TRIO amplification was not associated with poor prognosis. Using a frozen bladder tumor tissue microarray RNA in situ hybridization confirmed that TRIO is up-regulated in amplified tumors. It is concluded that TRIO up-regulation through amplification has a potential role in bladder cancer progression. Studies by comparative genomic hybridization (CGH) demonstrated gains and amplifications at many different chromosomal loci mainly in invasive bladder cancer. 1 Gene copy number increase is an important mechanism leading to abnormal expression of known oncogenes such as MYC at 8q24, CCND1 at 11q13, or HER2 at 17q21. 2-4 However, most of the chromosomal regions found amplified in bladder cancer 1 do not contain known oncogenes, suggesting that many amplification target genes remain to be identified.Amplifications of the short arm of chromosome 5 are of particular interest. In previous CGH studies 5p amplification was found to be one of the few alterations occurring more frequently in muscle invasive tumors (stage pT2 and higher) than in early invasive cancers (stage pT1). 5 Our hypothesis of a role of 5p amplification for bladder cancer progression was further corroborated by the results of a second CGH study finding a significant association between 5p amplifications and an increased risk for tumor progression in a series of pT1 carcinomas. 6 Because amplifications often cover large areas of 5p in bladder cancer, it is difficult to narrow down the region of amplification using positional cloning approaches. Based on our CGH studies, one of the most common sites of amplification is in the 5p15-p14 region. 5 In an attempt to find oncogene candidates among known genes allocated in this chromosomal area, we became interested in TRIO located at 5p15.2. 7 The TRIO protein contains a serine/threonine kinase domain and two guanine nucleotide exchange factor domains for the family of Rho-like GTPases, specific for Rac1 and RhoA. 8 These functional domains suggest that this enzyme may play a role in signaling pathways contro...

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Molecular cloning and chromosomal mapping of CCND genes encoding human D-type cyclins

Cited by 178 publications

References 29 publications

GSK3β mediates suppression of cyclin D2 expression by tumor suppressor PTEN

GSK3β mediates suppression of cyclin D2 expression by tumor suppressor PTEN

Increased cell growth and tumorigenicity in human prostate LNCaP cells by overexpression to cyclin D1

TRIO Amplification and Abundant mRNA Expression Is Associated with Invasive Tumor Growth and Rapid Tumor Cell Proliferation in Urinary Bladder Cancer

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