Reduced levels of E-cadherin correlate with progression of corticotroph pituitary tumours

Evang, Johan Arild; Berg, Jens Petter; Casar‐Borota, Olivera; Lekva, Tove; Kringen, Marianne Kristiansen; Ramm‐Pettersen, Jon; Bollerslev, Jens

doi:10.1111/j.1365-2265.2011.04109.x

Cited by 27 publications

(43 citation statements)

References 30 publications

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“…By contrast, E-cadherin mRNA levels were significantly reduced in invasive compared with non-invasive GH-secreting tumours. Alteration of E-cadherin expression has been shown in pituitary adenomas (8,19,40), is now well characterised in GH-producing adenomas (8,42,44,45) and is not correlated with pre-operative medical treatment (8). In the present study, we have observed that ESRP1 expression was significantly reduced in GH invasive tumours and E-cadherin expression was positively associated with that of ESRP1.…”

Section: Discussionsupporting

confidence: 48%

“…This process has multiple consequences for the phenotype and behaviour of cells, and constitutes one major aspect of the cancerrelated epithelial mesenchymal transition (EMT) process (18). Epithelial E-cadherin expression has been investigated in several pituitary adenoma subtypes and its alteration could contribute to the invasiveness of pituitary adenomas (8,19,20). In addition, molecular studies have suggested that EMT may play an important role in GH adenoma progression (21)(22)(23)(24).…”

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confidence: 99%

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Combining Cadherin Expression with Molecular Markers Discriminates Invasiveness in Growth Hormone and Prolactin Pituitary Adenomas

Chauvet

Romanò

Meunier

et al. 2016

J Neuroendocrinology

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Although growth hormone (GH)- and prolactin (PRL)-secreting pituitary adenomas are considered benign, in many patients, tumour growth and/or invasion constitute a particular challenge. In other tumours, progression relies in part on dysfunction of intercellular adhesion mediated by the large family of cadherins. In the present study, we have explored the contribution of cadherins in GH and PRL adenoma pathogenesis, and evaluated whether this class of adherence molecules was related to tumour invasiveness. We have first established, by quantitative polymerase chain reaction and immunohistochemistry, the expression profile of classical cadherins in the normal human pituitary gland. We show that the cadherin repertoire is restricted and cell-type specific. Somatotrophs and lactotrophs express mainly E-cadherin and cadherin 18, whereas N-cadherin is present in the other endocrine cell types. This repertoire undergoes major differential modification in GH and PRL tumours: E-cadherin is significantly reduced in invasive GH adenomas, and this loss is associated with a cytoplasmic relocalisation of cadherin 18 and catenins. In invasive prolactinomas, E-cadherin distribution is altered and is accompanied by a mislocalisation of cadherin 18, β-catenin and p120 catenin. Strikingly, de novo expression of N-cadherin is present in a subset of adenomas and cells exhibit a mesenchymal phenotype exclusively in invasive tumours. Binary tree analysis, performed by combining the cadherin repertoire with the expression of a subset of known molecular markers, shows that cadherin/catenin complexes play a significant role in discrimination of tumour invasion.

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Section: Discussionsupporting

confidence: 48%

mentioning

confidence: 99%

Combining Cadherin Expression with Molecular Markers Discriminates Invasiveness in Growth Hormone and Prolactin Pituitary Adenomas

Chauvet

Romanò

Meunier

et al. 2016

J Neuroendocrinology

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“…EMT is shown to be of significant importance in the aggressiveness and progression of somatotroph and corticotroph adenomas (15,17,18). However, using our selection criteria, we cannot conclude that EMT is the major component of the tumor growth in gonadotroph adenomas.…”

Section: Discussionmentioning

confidence: 82%

“…Studies of growth hormone and ACTH-producing adenomas have linked EMT to the progression of tumors. The reduction in E-cadherin content in these tumors has been associated with tumor size, invasiveness and poor response to medical treatment (15,17,18,19,20).…”

Section: Introductionmentioning

confidence: 99%

Gene expression profiling of fast- and slow-growing non-functioning gonadotroph pituitary adenomas

Falch

Sundaram

Øystese

et al. 2018

European Journal of Endocrinology

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“…Studies by Qian et al (2007) found a somewhat lower percentage of tumors with reduced E-cadhein expression, 62% of 69 tumors. Evang et al (2011) investigated 48 ACTH-secreting tumors and found that 77% of them had lost or had significantly reduced E-cadherin. Fougner et al (2010) found that the percentage was 47% in GH-tumors ( n = 83).…”

Section: The Rb Connectionmentioning

confidence: 99%

Genetic and epigenetic mutations of tumor suppressive genes in sporadic pituitary adenoma

Zhou

Zhang

Klibanski

2014

Molecular and Cellular Endocrinology

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Human pituitary adenomas are the most common intracranial neoplasms. Approximately 5% of them are familial adenomas. Patients with familial tumors carry germline mutations in predisposition genes, including AIP, MEN1 and PRKAR1A. These mutations are extremely rare in sporadic pituitary adenomas, which therefore are caused by different mechanisms. Multiple tumor suppressive genes linked to sporadic tumors have been identified. Their inactivation is caused by epigenetic mechanisms, mainly promoter hypermethylation, and can be placed into two groups based on their functional interaction with tumor suppressors RB or p53. The RB group includes CDKN2A, CDKN2B, CDKN2C, RB1, BMP4, CDH1, CDH13, GADD45B and GADD45G; AIP and MEN1 genes also belong to this group. The p53 group includes MEG3, MGMT, PLAGL1, RASSF1, RASSF3 and SOCS1. We propose that the tumor suppression function of these genes is mainly mediated by the RB and p53 pathways. We also discuss possible tumor suppression mechanisms for individual genes.

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Reduced levels of E-cadherin correlate with progression of corticotroph pituitary tumours

Abstract: Corticotroph tumour progression was associated with reduced expression of the epithelial marker E-cadherin.

Cited by 27 publications

References 30 publications

Combining Cadherin Expression with Molecular Markers Discriminates Invasiveness in Growth Hormone and Prolactin Pituitary Adenomas

Combining Cadherin Expression with Molecular Markers Discriminates Invasiveness in Growth Hormone and Prolactin Pituitary Adenomas

Gene expression profiling of fast- and slow-growing non-functioning gonadotroph pituitary adenomas

Genetic and epigenetic mutations of tumor suppressive genes in sporadic pituitary adenoma

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