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Regulation of E-cadherin/Catenin Association by Tyrosine Phosphorylation*
TLDR
Transient transfections of different mutants demonstrated that Tyr-654 is phosphorylated in conditions in which adherens junctions are disrupted and evidenced that binding ofβ-catenin to E-cadherin in vivo is controlled by phosphorylation of β- catenin Tyr-652.
Snail Induction of Epithelial to Mesenchymal Transition in Tumor Cells Is Accompanied by MUC1 Repression andZEB1 Expression*
TLDR
ZEB1 and Snail had a similar pattern of expression in epithelial cell lines, and both were induced by overexpression of ILK1, a kinase that causes the loss of E-cadherin and the acquisition of a fibroblastic phenotype.
A natural antisense transcript regulates Zeb2/Sip1 gene expression during Snail1-induced epithelial-mesenchymal transition.
TLDR
The results presented in this article reveal the existence of a NAT capable of activating Zeb2 expression, explain the mechanism involved in this activation, and demonstrate that this NAT regulates E-cadherin expression.
Vitamin D3 promotes the differentiation of colon carcinoma cells by the induction of E-cadherin and the inhibition of β-catenin signaling
TLDR
1α,25(OH)2D3 induces E-cadherin and modulates β-catenin–TCF-4 target genes in a manner opposite to that of β- catenin, promoting the differentiation of colon carcinoma cells.
Functional Cooperation between Snail1 and Twist in the Regulation of ZEB1 Expression during Epithelial to Mesenchymal Transition*
TLDR
Results indicate that Snail1 controls Zeb1 expression at multiple levels and acts cooperatively with Twist in the ZEB1 gene transcription induction, showing a mutual dependence although to a different extent.
Regulation of beta-catenin structure and activity by tyrosine phosphorylation.
TLDR
The results explain how phosphorylation of beta-catenin in Tyr-654 modifies the tertiary structure of this protein and the interaction with its different partners.
Epithelial-mesenchymal transition can suppress major attributes of human epithelial tumor-initiating cells.
TLDR
Two human cellular models derived from prostate and bladder cancer provide new insights into how dynamic interactions among epithelial, self-renewal, and mesenchymal gene programs determine the plasticity of epithelial TICs.
Loss of E-cadherin Expression in Melanoma Cells Involves Up-regulation of the Transcriptional Repressor Snail*
TLDR
It is concluded that activation of Snail expression plays an important role in down-regulation of E-cadherin and tumorigenesis of malignant melanomas.
Functional Heterogeneity of Cancer-Associated Fibroblasts from Human Colon Tumors Shows Specific Prognostic Gene Expression Signature
TLDR
The heterogeneity of primary CAFs' effect on colon cancer cell migration is shown for the first time, and a CAF gene expression signature able to classify patients with colon cancer into high- and low-risk groups was identified.
The Hypoxia-controlled FBXL14 Ubiquitin Ligase Targets SNAIL1 for Proteasome Degradation*
TLDR
It is demonstrated that the F-box E3 ubiquitin ligase FBXl14 interacts with SNAIL1 and promotes its ubiquitylation and proteasome degradation independently of phosphorylation by GSK-3β, suggesting that additional E3 ligases participate in the control of SNAil1 protein stability.
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