β-Catenin and ZO-1: Shuttle Molecules Involved in Tumor Invasion-Associated Epithelial-Mesenchymal Transition Processes

Polette, Myriam; Mestdagt, Mélanie; Bindels, S; Nawrocki‐Raby, Béatrice; Hunziker, Walter; Foidart, Jean‐Michel; Birembaut, Philippe; Gilles, Christine

doi:10.1159/000101304

Cited by 116 publications

(98 citation statements)

References 67 publications

(30 reference statements)

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“…In contrast, the localisation of vimentin in both control and EGF-treated cells remained filamentous ( Figure 2D). However, EGF treatment resulted in the translocation of b-catenin from the cytoplasm and cell junctions to discrete regions of the nucleus in certain population of cells ( Figure 2E), consistent with the activation of the b-catenin-mediated pathways in response to EGF-associated EMT events (Polette et al, 2007).…”

Section: Jak2/stat3 Status In Ovarian Carcinomassupporting

confidence: 75%

Cross talk of signals between EGFR and IL-6R through JAK2/STAT3 mediate epithelial–mesenchymal transition in ovarian carcinomas

et al. 2008

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Epidermal growth factor receptor (EGFR) is overexpressed in ovarian carcinomas, with direct or indirect activation of EGFR able to trigger tumour growth. We demonstrate significant activation of both signal transducer and activator of transcription (STAT)3 and its upstream activator Janus kinase (JAK)2, in high-grade ovarian carcinomas compared with normal ovaries and benign tumours. The association between STAT3 activation and migratory phenotype of ovarian cancer cells was investigated by EGF-induced epithelialmesenchymal transition (EMT) in OVCA 433 and SKOV3 ovarian cancer cell lines. Ligand activation of EGFR induced a fibroblast-like morphology and migratory phenotype, consistent with the upregulation of mesenchyme-associated N-cadherin, vimentin and nuclear translocation of b-catenin. This occurred concomitantly with activation of the downstream JAK2/STAT3 pathway. Both cell lines expressed interleukin-6 receptor (IL-6R), and treatment with EGF within 1 h resulted in a several-fold enhancement of mRNA expression of IL-6. Consistent with that, EGF treatment of both OVCA 433 and SKOV3 cell lines resulted in enhanced IL-6 production in the serum-free medium. Exogenous addition of IL-6 to OVCA 433 cells stimulated STAT3 activation and enhanced migration. Blocking antibodies against IL-6R inhibited IL-6 production and EGF-and IL-6-induced migration. Specific inhibition of STAT3 activation by JAK2-specific inhibitor AG490 blocked STAT3 phosphorylation, cell motility, induction of N-cadherin and vimentin expression and IL6 production. These data suggest that the activated status of STAT3 in high-grade ovarian carcinomas may occur directly through activation of EGFR or IL-6R or indirectly through induction of IL-6R signalling. Such activation of STAT3 suggests a rationale for a combination of anti-STAT3 and EGFR/IL-6R therapy to suppress the peritoneal spread of ovarian cancer.

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Section: Jak2/stat3 Status In Ovarian Carcinomassupporting

confidence: 75%

Cross talk of signals between EGFR and IL-6R through JAK2/STAT3 mediate epithelial–mesenchymal transition in ovarian carcinomas

et al. 2008

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“…To further examine whether Dicer is required in cell-cell adhesion, expression and distribution of the tight junction protein ZO-1 (zona occludens-1, encoded by the Tjp1 gene) was analyzed on cultured epicardial cells. Translocation of ZO-1 between the cell surface and cytoplasm has been implicated in EMT (33). In control epicardial explants, ZO-1 expression was weak and diffuse, and its distribution was not restricted to the cell surface, a hallmark of cells undergoing EMT (Fig.…”

Section: Epicardial Deletion Of Dicer Leads To Perinatalmentioning

confidence: 96%

MicroRNA-processing Enzyme Dicer Is Required in Epicardium for Coronary Vasculature Development

Singh

Lü

Massera

et al. 2011

Journal of Biological Chemistry

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Background: Epicardium-derived cells undergo EMT and differentiate into smooth muscle of the developing coronary vasculature. The role of Dicer in this process is unknown. Results: Dicer mutants displayed impaired epicardial EMT, reduced epicardial cell proliferation, and differentiation into coronary smooth muscle cells. Conclusion: Dicer is essential for epicardium development. Significance: This represents the first evidence for the involvement of Dicer, and by implication miRNAs, in epicardial development.

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“…The Wnt/β-catenin pathway is fundamental in the epithelial-mesenchymal transition (EMT), an important step in oncogenic transformation, which includes cell invasion and metastasis (36)(37)(38). The nuclear translocation of β-catenin leads to the downregulation of E-cadherin and subsequent induction of EMT (39), whereas the upregulation of β-catenin is associated with the invasion and metastasis of several types of solid tumor (40)(41)(42). A previous study found that TRIM24 knockdown decreased the levels of EMT-associated factors in hepatocellular carcinoma.…”

Section: A B C D E Fmentioning

confidence: 99%

TRIM24 promotes the aggression of gastric cancer via the Wnt/β-catenin signaling pathway

et al. 2017

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Abstract. Tripartite motif-containing 24 (TRIM24) is important in tumor development and progression. However, the role of TRIM24 in gastric cancer (GC) and the mechanisms underlying the dysregulated expression of TRIM24 remain to be fully elucidated. In the present study, it was found that TRIM24 was frequently overexpressed in GC cell lines and tissues compared with normal controls, as determined by western blotting and immunohistochemical staining. The high nuclear expression of TRIM24 was correlated with the depth of invasion (P=0.007), tumor-node-metastasis stage (P=0.005), and lymph node metastasis (P=0.027), and shorter overall survival rates (P=0.010) in patients with GC. Small interfering RNA-mediated knockdown of TRIM24 inhibited cell proliferation, colony formation, migration, invasion and the nuclear accumulation of β-catenin, and it delayed cell cycle progression and induced apoptosis. In addition, the expression of TRIM24 was positively correlated with that of β-catenin in GC tissues. TRIM24 knockdown decreased the expression of Wnt/β-catenin target genes, whereas the activation of Wnt/β-catenin signaling by lithium chloride reversed the effects of TRIM24 knockdown. Taken together, these data suggested that TRIM24 was a prognostic or potential therapeutic target for patients with GC and was important in the activation of the Wnt/β-catenin pathway during the progression of GC.

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β-Catenin and ZO-1: Shuttle Molecules Involved in Tumor Invasion-Associated Epithelial-Mesenchymal Transition Processes

Cited by 116 publications

References 67 publications

Cross talk of signals between EGFR and IL-6R through JAK2/STAT3 mediate epithelial–mesenchymal transition in ovarian carcinomas

Cross talk of signals between EGFR and IL-6R through JAK2/STAT3 mediate epithelial–mesenchymal transition in ovarian carcinomas

MicroRNA-processing Enzyme Dicer Is Required in Epicardium for Coronary Vasculature Development

TRIM24 promotes the aggression of gastric cancer via the Wnt/β-catenin signaling pathway

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