Genetic and protein changes of E-cadherin in meningiomas

Pećina‐Šlaus, Nives; Martić, Tamara Nikuševa; Deák, Ádám; Zeljko, Martina; Hrašćan, Reno; Tomas, Davor; Musani, Vesna

doi:10.1007/s00432-009-0708-z

Cited by 28 publications

(27 citation statements)

References 27 publications

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“…SFRP3, another Wnt pathway antagonist, reduces activity of metalloproteinases and activation of β-catenin and thus inhibits epithelial-mesenchymal transition (EMT) seen in several cancer types [22,23]. We observed statistically significant decreased of the amount of SFRP3 protein expression in our total renal cancer clear cell tumors compared with normal kidney tissues.…”

Section: Discussionmentioning

confidence: 56%

Expression of Secreted Frizzled-Related Protein 1 and 3, T-cell Factor 1 and Lymphoid Enhancer Factor 1 in Clear Cell Renal Cell Carcinoma

Nikuševa-Martić

Šerman

Zeljko

et al. 2013

Pathol. Oncol. Res.

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Frequency and mortality of renal cell carcinoma (RCC) are increasing for decades. However, the molecular background of RCC tumorigenesis is still poorly understood. In current study we investigated the expression of TCF/LEF and SFRP family members (SFRP1 and SFRP3)to gain a better understanding of biological signaling pathways responsible for epidemiology and clinical parameters of clear cell RCC (cRCC).36 pairs of paraffin-embedded clear cRCC and adjacent nontumoral tissues samples using immunohistochemistry (IHC) were analyzed and compared with corresponding clinicopathological parameters.Immunohistochemistry indicated statistically significant decreased SFRP3 expression in tumor tissues but no consistency in SFRP1 expression in analyzed normal and tumor tissue.The TCF1 expression level was significantly weaker in normal tissue compared to tumor samples while LEF1 protein levels were significantly weaker in tumor tissue.To our knowledge, this is the first report on analysis of the expression of transcription factors TCF1 and LEF1 in clear cell renal cell carcinoma and their comparison with Wnt signal pathway antagonists belonging to SFRP family.

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Section: Discussionmentioning

confidence: 56%

Expression of Secreted Frizzled-Related Protein 1 and 3, T-cell Factor 1 and Lymphoid Enhancer Factor 1 in Clear Cell Renal Cell Carcinoma

Nikuševa-Martić

Šerman

Zeljko

et al. 2013

Pathol. Oncol. Res.

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“…In esophageal squamous cell carcinoma (ESCC), overexpression of FRAT1 is associated with increased cell proliferation and aberrant activation of the β-catenin/TCF pathway, a consequence of nuclear accumulation of β-catenin that promotes the transcriptional activity of β-catenin/TCF [34]. Interestingly, also higher-grade meningiomas exhibit increased protein level and nuclear/perinuclear localization of β-catenin [31, 35], suggesting aberrant activation of the Wnt signaling pathway [9]. In gliomas, overexpression of FRAT1 is correlated with a malignant phenotype, higher cell proliferation, decreased apoptosis and poor prognosis [36, 37].…”

Section: Discussionmentioning

confidence: 99%

“…This observation is consistent with our result that downregulation of miR-34a-3p reduced apoptosis of meningioma cells in vitro . The exhibited nuclear accumulation of β-catenin in higher-grade meningiomas [31, 35] may be, in part, due to loss of translational repression of FRAT1 due to the decreased levels of miR-34a-3p.…”

Section: Discussionmentioning

confidence: 99%

MiR-34a-3p alters proliferation and apoptosis of meningioma cells in vitro and is directly targeting SMAD4, FRAT1 and BCL2

Werner

Hart

Nickels

et al. 2017

Aging

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Micro (mi)RNAs are short, noncoding RNAs and deregulation of miRNAs and their targets are implicated in tumor generation and progression in many cancers. Meningiomas are mostly benign, slow growing tumors of the central nervous system with a small percentage showing a malignant phenotype.Following in silico prediction of potential targets of miR-34a-3p, SMAD4, FRAT1, and BCL2 have been confirmed as targets by dual luciferase assays with co-expression of miR-34a-3p and reporter gene constructs containing the respective 3'UTRs. Disruption of the miR-34a-3p binding sites in the 3'UTRs resulted in loss of responsiveness to miR-34a-3p overexpression. In meningioma cells, overexpression of miR-34a-3p resulted in decreased protein levels of SMAD4, FRAT1 and BCL2, while inhibition of miR-34a-3p led to increased levels of these proteins as confirmed by Western blotting. Furthermore, deregulation of miR-34a-3p altered cell proliferation and apoptosis of meningioma cells in vitro.We show that SMAD4, FRAT1 and BCL2 are direct targets of miR-34a-3p and that deregulation of miR-34a-3p alters proliferation and apoptosis of meningioma cells in vitro. As part of their respective signaling pathways, which are known to play a role in meningioma genesis and progression, deregulation of SMAD4, FRAT1 and BCL2 might contribute to the aberrant activation of these signaling pathways leading to increased proliferation and inhibition of apoptosis in meningiomas.

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“…Since beta-catenin is an integral part of the C-terminal intracellular complex of E-cadherin therefore E-cadherin is indirectly involved in the relevant cancerrelated pathophysiology [36]. A recent study using 60 meningioma tissues revealed sporadic E-cadherin expression in the tumors that further strengthen our understanding of the role of E-cadherin in meningiomas [37].…”

Section: E-cadherin In Nerve-tissue Cancermentioning

confidence: 90%

The Curses and the Blesses of E-Cadherin

Akaike¹

2014

Human Genet Embryol

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E-cadherin is an evolutionary conserved molecule expressing from lower level animal to human. The principal role of E-cadherin is to maintain appropriate cell-cell connectivity at adherensjunction. Besides its role as cell-cell connector protein, E-cadherin is integrally involved in intracellular signaling as well as cytoskeletal remodeling. Proper spaciotemporal regulations as well as relevant specialized functions of E-cadherin are important for maintaining normal embryogenesis, cellular morphology and physiological function. However, defects in the expression and function of this gene products could become curses since numerous genetic and developmental studies have identified the critical role of this gene in path physiological conditions of multiple types of cancers leading to fatality. Recent study identified essential role of this gene product in stem cell biology including normal embryogenesis, induced pluripotent stem cell (iPSC) generation and stem cell differentiation. Currently iPSC has become a prime choice as starting material for regenerative medicine to treat many diseases; however the relevant technology has many shortcomings. Our lab and others have been exploiting this protein for successful application in regenerative medicine that made it a blessed molecule. Here, based on the latest available information, we are concisely presenting these agonies and advantages of E-cadherin.

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Genetic and protein changes of E-cadherin in meningiomas

Abstract: Our results suggest that genetic instabilities of the E-cadherin gene have a role in meningioma development and progression. Detected microsatellite instability indicates that mismatch repair may also be targeted in meningioma.

Cited by 28 publications

References 27 publications

Expression of Secreted Frizzled-Related Protein 1 and 3, T-cell Factor 1 and Lymphoid Enhancer Factor 1 in Clear Cell Renal Cell Carcinoma

Expression of Secreted Frizzled-Related Protein 1 and 3, T-cell Factor 1 and Lymphoid Enhancer Factor 1 in Clear Cell Renal Cell Carcinoma

MiR-34a-3p alters proliferation and apoptosis of meningioma cells in vitro and is directly targeting SMAD4, FRAT1 and BCL2

The Curses and the Blesses of E-Cadherin

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