Pituitary tumour transforming gene (PTTG) expression correlates with the proliferative activity and recurrence status of pituitary adenomas: a clinical and immunohistochemical study

Filippella, Mariagiovanna; Galland, F.; Kujas, M.; Young, Jacques; Faggiano, Antongiulio; Lombardi, Gaetano; Colao, Annamaria; Meduri, Géri; Chanson, Philippe

doi:10.1111/j.1365-2265.2006.02630.x

Cited by 141 publications

(84 citation statements)

References 64 publications

(89 reference statements)

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“…PTTG and MMP9 were also up-regulated in the invasive tumors, as measured by qRT-PCR (data not shown), in keeping with previous findings (Turner et al 2000, Trouillas et al 2003, Filippella et al 2006, Gong et al 2008, Hussaini et al 2007, Wierinckx et al 2007. At the protein level, PTTG staining was stronger in invasive tissues and displayed a good correlation with that of MYO5A.…”

Section: Igfbp5supporting

confidence: 77%

“…In our series, Ki67 immunostaining was similar in invasive and non-invasive NFPAs, but the predictiveness of the Ki67 labeling index for aggressive behavior is greater in functioning pituitary adenomas (including prolactinomas) than in NFPAs (Gurlek et al 2007). Moreover, we have previously shown that the Ki67 labeling index is more reliable for predicting the recurrence of pituitary tumors (Filippella et al 2006).…”

Section: Igfbp5mentioning

confidence: 99%

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Differential gene expression profiles of invasive and non-invasive non-functioning pituitary adenomas based on microarray analysis

Galland¹,

Lacroix²,

Saulnier³

et al. 2010

Endocrine-Related Cancer

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Non-functioning pituitary adenomas (NFPAs) may be locally invasive. Markers of invasiveness are needed to guide patient management and particularly the use of adjuvant radiotherapy. To examine whether invasive NFPAs display a specific gene expression profile relative to non-invasive tumors, we selected 40 NFPAs (38 of the gonadotroph type) and classified them as invasive (nZ22) or non-invasive (nZ18) on the basis of magnetic resonance imaging and surgical findings. We then performed pangenomic analysis with the 44k Agilent human whole genome expression oligonucleotide microarray in order to identify genes with differential expression between invasive and non-invasive NFPAs. Candidate genes were then tested in qRT-PCR. Prediction class analysis showed that the expression of 346 genes differed between invasive and non-invasive NFPAs (P!0.001), of which 233 genes were up-regulated and 113 genes were down-regulated in invasive tumors. On the basis of Ingenuity networks and the degree of up-or down-regulation in invasive versus non-invasive tumors, 35 genes were selected for expression quantification by qRT-PCR. Overexpression of only four genes was confirmed, namely IGFBP5 (PZ0.02), MYO5A (PZ0.04), FLT3 (PZ0.01), and NFE2L1 (PZ0.02). At the protein level, only myosin 5A (MYO5A) immunostaining was stronger in invasive than in non-invasive NFPAs. Molecular signature allows to differentiate 'grossly' invasive from non-invasive NFPAs. The product of one of these genes, MYO5A, may be a useful marker of tumor invasiveness.

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Section: Igfbp5supporting

confidence: 77%

Section: Igfbp5mentioning

confidence: 99%

Differential gene expression profiles of invasive and non-invasive non-functioning pituitary adenomas based on microarray analysis

Galland¹,

Lacroix²,

Saulnier³

et al. 2010

Endocrine-Related Cancer

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“…PTTG1 was also identified as human securin, a critical regulator of sister chromatid separation in late stage mitosis (19,20). PTTG1 is expressed at very low or undetectable levels in most normal human tissues but is abundantly expressed in malignant cell lines and pituitary tumors (18,(21)(22)(23). However, the mechanisms by which PTTG1 contributes to tumor progression are not well understood.…”

mentioning

confidence: 99%

PTTG1 Oncogene Promotes Tumor Malignancy via Epithelial to Mesenchymal Transition and Expansion of Cancer Stem Cell Population

Yoon

Kim

Lee

et al. 2012

Journal of Biological Chemistry

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Background: PTTG1 is an oncogene with its expression levels correlating with tumor development and metastasis. Results: Modulation of PTTG1 expression levels revealed that PTTG1 promotes invasive and migratory properties and expansion of CD44 high CD24 low cell population via AKT activation in breast cancer cells. Conclusion: PTTG1 induces EMT and promotes cancer stem cells via activation of AKT. Significance: PTTG1 represents a potential target for therapeutic intervention against the spread of breast cancer.

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“…Oct-1 and hPTTG1 are concordantly expressed in endocrine tumors and colon cancers hPTTG1 is overexpressed in multiple human tumors including pituitary, breast, and colorectal tumors (Zhang et al 1999a, Solbach et al 2004, Filippella et al 2006. High Oct-1 protein expression was detected in gastric carcinomas (Almeida et al 2005).…”

Section: Zhou Et Al: Oct-1 Induces Hpttg1 Expressionmentioning

confidence: 99%

“…hPTTG1 abundance or loss of function (Jallepalli et al 2001, Wang et al 2001 both result in abnormal mitosis and chromosomal instability. In contrast to restricted normal tissue expression, hPTTG1 is upregulated in pituitary (Zhang et al 1999a, Filippella et al 2006, thyroid (Kim et al 2006), breast (Solbach et al 2004), esophageal (Shibata et al 2002), and colorectal tumors . The hPTTG1 overexpression correlates with tumor invasiveness, differentiation, tumor recurrence, and prognosis.…”

Section: Introductionmentioning

confidence: 99%

Oct-1 induces pituitary tumor transforming gene expression in endocrine tumors

Zhou

Tong²,

Wawrowsky³

et al. 2008

Endocrine Related Cancer

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As human pituitary tumor transforming gene (hPTTG1) is upregulated in endocrine tumors, we studied regulatory mechanisms for hPTTG1 expression. We identified Oct-1-binding motifs in the hPTTG1 promoter region and show Oct-1-specific binding to the hPTTG1 promoter using chromatin immunoprecipitation. We overexpressed Oct-1 and observed w2.5-fold activation of hPTTG1 promoter luciferase constructs (K2642/K1 and K1717/K1). Transcriptional activation was abrogated by co-transfection of an inactive Oct-1 form lacking the POU domain or by utilizing mutated hPTTG1 promoters or mutants devoid of two Oct-1-binding motifs (K1717/K1mut, K637/K1 or K433/K1). Using biotin-streptavidin pull-down assays, we confirmed Oct-1 binding to the two octamer motifs in the hPTTG1 promoter (K1669/K1631 and K1401/K1361). Endogenous hPTTG1 mRNA and protein increased up to approximately fourfold in Oct-1 transfectants, as measured by real-time PCR and western blot. In contrast, siRNA-mediated suppression of endogenous Oct-1 attenuated both the hPTTG1 mRNA and protein levels. Using confocal immunofluorescence imaging, Oct-1 and hPTTG1 were concordantly upregulated in pituitary (57 and 62%, nZ79, P!0.01) and breast tumor specimens (57 and 42%, nZ77, P!0.05) respectively. The results show that Oct-1 transactivates hPTTG1, and both proteins are concordantly overexpressed in endocrine tumors, thus offering a mechanism for endocrine tumor hPTTG1 abundance.

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Pituitary tumour transforming gene (PTTG) expression correlates with the proliferative activity and recurrence status of pituitary adenomas: a clinical and immunohistochemical study

Cited by 141 publications

References 64 publications

Differential gene expression profiles of invasive and non-invasive non-functioning pituitary adenomas based on microarray analysis

Differential gene expression profiles of invasive and non-invasive non-functioning pituitary adenomas based on microarray analysis

PTTG1 Oncogene Promotes Tumor Malignancy via Epithelial to Mesenchymal Transition and Expansion of Cancer Stem Cell Population

Oct-1 induces pituitary tumor transforming gene expression in endocrine tumors

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