Molecular cloning of pituitary tumor transforming gene 1 from ovarian tumors and its expression in tumors

Puri, Rashmi; Tousson, Albert; Chen, Leilei; Kakar, Sham S.

doi:10.1016/s0304-3835(00)00688-1

Cited by 72 publications

(73 citation statements)

References 20 publications

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“…On the basis of structural homology, PTTG1 protein was identified as a vertebrate securin involved in the regulation of sister chromatid separation during mitosis. It has been reported that the PTTG1 was highly expressed in various tumors [Heaney et al, 2000[Heaney et al, , 2001Puri et al, 2001;Solbach et al, 2004] and ectopic overexpression of this gene caused cellular transformation in vitro [Zhang et al, 1999;Hamid et al, 2005]. In our microarray experiment, the PTTG1 was upregulated by the exposures of all three carcinogens that have different carcinogenic mechanisms.…”

Section: Discussionsupporting

confidence: 48%

Comparison of gene expression profiles in HepG2 cells exposed to arsenic, cadmium, nickel, and three model carcinogens for investigating the mechanisms of metal carcinogenesis

Kawata

Shimazaki

Okabe

2008

Environ and Mol Mutagen

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Carcinogenesis is an important chronic toxicity of metals and metalloids, although their mechanisms of action are still unclear. Comparison of gene expression patterns induced by carcinogenic metals, metalloids, and model carcinogens would give an insight into understanding of their carcinogenic mechanisms. In this study, we examined the gene expression alteration in human hepatoma cell line, HepG2, after exposing to two metals (cadmium and nickel), a metalloid (arsenic), and three model carcinogenic chemicals N-dimethylnitrosoamine (DMN), 12-O-tetradecanoylphorbol-13-acetate (TPA), and tetrachloroethylene (TCE) using DNA microarrays with 8,795 human genes. Of the genes altered by As, Cd, and Ni exposures, 31-55% were overlapped with those altered by three model carcinogenic chemical exposures in our experiments. In particular, the metals and metalloid shared certain characteristics with TPA and TCE in remarkable upregulations of the genes associated with progression of cell cycle, which might play a central role in As, Cd, and Ni carcinogenesis. This characteristic of gene expression alteration was partially counteracted by intracellular accumulation of vitamin C in Asexposed cells, whereas the number of cell-cycle associated genes was increased in Cd-and Niexposed cells. In our experimental conditions, ROS might have an accelerative effect on the cell proliferation mechanisms of As, but have an inhibitory effect on those of other two heavy metals. Furthermore, based on the results of Q-PCR, the oncogene PTTG1, which was upregulated by all carcinogenic chemical exposures in the array experiments, might be a useful biomarker for evaluation of the carcinogenesis of inorganic carcinogens. Environ. Mol. Mutagen. 50:46-59, 2009.

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Section: Discussionsupporting

confidence: 48%

Comparison of gene expression profiles in HepG2 cells exposed to arsenic, cadmium, nickel, and three model carcinogens for investigating the mechanisms of metal carcinogenesis

Kawata

Shimazaki

Okabe

2008

Environ and Mol Mutagen

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“…Subcutaneous injection of PTTG1-transfected cells into nude mice has been shown to induce tumors formation. Furthermore, PTTG1 overexpression has been reported in many human tumors (10)(11)(12)(13)(14)(15)(16)(17)(18). PTTG1 is involved in several cellular processes, including DNA damage repair, apoptosis, and angiogenesis.…”

Section: Introductionmentioning

confidence: 99%

Prostate Cancer Cell Response to Paclitaxel Is Affected by Abnormally Expressed Securin PTTG1

Castilla

Medina

et al. 2014

Molecular Cancer Therapeutics

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PTTG1 protein, the human securin, has a central role in sister chromatid separation during mitosis, and its altered expression has been reported in many tumor types. Paclitaxel is a widely used chemotherapeutic drug, whose mechanism of action is related to its ability to arrest cells in mitosis and the subsequent induction of the intrinsic apoptotic pathway. By using two prostate cancer cell lines with different responses to paclitaxel treatment, we have identified two situations in which PTTG1 influences cell fate differentially. In slippageprone PC3 cells, both PTTG1 downregulation and overexpression induce an increase in mitotic cells that is associated with diminished apoptosis after paclitaxel treatment. In LNCaP cells, however, PTTG1 downregulation prevents mitotic entry and, subsequently, inhibits mitosis-associated, paclitaxel-induced apoptosis. In contrast, PTTG1 overexpression induces an increase in mitotic cells and apoptosis after paclitaxel treatment. We have also identified a role for Mcl-1 protein in preventing apoptosis during mitosis in PC3 cells, as simultaneous PTTG1 and Mcl-1 silencing enhances mitosis-associated apoptosis after paclitaxel treatment. The finding that a more efficient mitotic arrest alone in PC3 cells is not enough to increase apoptosis was also confirmed with the observation that a selected paclitaxel-resistant PC3 cell line showed an apoptosis-resistant phenotype associated with increased mitosis upon paclitaxel treatment. These findings could contribute to identify putative responsive and nonresponsive cells and help us to approach incomplete responses to paclitaxel in the clinical setting. Mol Cancer Ther; 13(10); 2372-83. Ó2014 AACR.

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“…PTTG is a multifunctional human securin, with a role in the control of mitosis (Zou et al, 1999;Yu et al, 2000;Zur and Brandeis, 2001), cell transformation (Pei and Melmed, 1997;Zhang et al, 1999b), DNA repair (Romero et al, 2001), gene regulation (Zhang et al, 1999b;Pei, 2000;McCabe et al, 2002) and fetal development (Boelaert et al, 2003b). PTTG overexpression has been reported in tumours of the thyroid , pituitary (Zhang et al, 1999a;McCabe et al, 2003), colon (Heaney et al, 2000), ovary (Puri et al, 2001) and breast (Puri et al, 2001), as well as in haematopoietic neoplasms (Dominguez et al, 1998). In thyroid, pituitary, oesophageal and colorectal tumours, high PTTG expression correlates with poor prognosis (Zhang et al, 1999a;Heaney et al, 2000;Shibata et al, 2002;Boelaert et al, 2003a;McCabe et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

PTTG and PBF repress the human sodium iodide symporter

et al. 2007

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The ability of the thyroid to accumulate iodide provides the basis for radioiodine ablation of differentiated thyroid cancers and their metastases. Most thyroid tumours exhibit reduced iodide uptake, although the mechanisms accounting for this remain poorly understood. Pituitary tumour transforming gene (PTTG) is a proto-oncogene implicated in the pathogenesis of thyroid tumours. We now show that PTTG and its binding factor PBF repress expression of sodium iodide symporter (NIS) messenger RNA (mRNA), and inhibit iodide uptake. This process is mediated at least in part through fibroblast growth factor-2. In detailed studies of the NIS promoter in rat FRTL-5 cells, PTTG and PBF demonstrated specific inhibition of promoter activity via the human upstream enhancer element (hNUE). Within this B1 kb element, a complex PAX8-upstream stimulating factor 1 (USF1) response element proved critical both to basal promoter activity and to PTTG and PBF repression of NIS. In particular, repression by PTTG was contingent upon the USF1, but not the PAX8, site. Finally, in human primary thyroid cells, PTTG and PBF similarly repressed the NIS promoter via hNUE. Taken together, our data suggest that the reported overexpression of PTTG and PBF in differentiated thyroid cancer has profound implications for activity of the NIS gene, and hence significantly impacts upon the efficacy of radioiodine treatment.

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Molecular cloning of pituitary tumor transforming gene 1 from ovarian tumors and its expression in tumors

Cited by 72 publications

References 20 publications

Comparison of gene expression profiles in HepG2 cells exposed to arsenic, cadmium, nickel, and three model carcinogens for investigating the mechanisms of metal carcinogenesis

Comparison of gene expression profiles in HepG2 cells exposed to arsenic, cadmium, nickel, and three model carcinogens for investigating the mechanisms of metal carcinogenesis

Prostate Cancer Cell Response to Paclitaxel Is Affected by Abnormally Expressed Securin PTTG1

PTTG and PBF repress the human sodium iodide symporter

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