E-cadherin

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E-cadherin variants associated with oral facial clefts trigger aberrant cell motility in a REG1A dependent manner

The i3S Epithelial Interactions in Cancer group coordinated a multidisciplinary team to address how germline alterations of E-cadherin trigger different clinical manifestations. The group was intrigued by the fact that loss of E-cadherin function may cause hereditary diffuse gastric cancer (HDGC) and congenital malformations, such as orofacial clefts (OFC).

Fatores e biomarcadores que explicam as disparidades na sobrevida de doentes com cancro gástrico em estadios precoces entre o mundo oriental e ocidental

A ressecção cirúrgica e a quimioterapia perioperatória são a base universal para o tratamento curativo de doentes com cancro do estômago. No entanto, a sobrevida dos doentes com cancro do estômago nas regiões do mundo ocidental e oriental continua a ser muito distinta.

Factors and biomarkers explaining disparities in survival outcomes of early stage gastric cancer between western and eastern world regions

Multidisciplinary research presents new protocol for the functional characterization of missense type mutations in the gene coding for the adhesion molecule E-cadherin.

Authors and Affiliations:

Soraia Melo 1,2,3, Joana Figueiredo 1,2, Maria Sofia Fernandes 1,2,4, Margarida Gonçalves 1,5, Eurico Morais-de-Sá 1,5, João Miguel Sanches 4 and Raquel Seruca 1,2,3

1 Instituto de Investigação e Inovação em Saúde (i3S), University of Porto, 4200-135 Porto, Portugal

2 Institute of Molecular Pathology and Immunology, University of Porto (IPATIMUP), 4200-135 Porto, Portugal

O–mannosylation and N-glycosylation: two coordinated mechanisms regulating the tumour suppressor functions of E-cadherin in cancer

E-cadherin-defective gastric cancer cells depend on Laminin to survive and invade

Authors and Affiliations:
Caldeira J 1*, Figueiredo J 2*, Brás-Pereira C 3, Carneiro P 2, Moreira AM 2, Pinto MT 2, Relvas JB 4, Carneiro F 5, Barbosa M 6, Casares F 7, Janody F 3, Seruca R 8.
*The authours contributed equally

Preventing E-cadherin aberrant N-glycosylation at Asn-554 improves its critical function in gastric cancer

Hereditary Diffuse Gastric Cancer Syndrome CDH1 Mutations and Beyond

Hereditary Diffuse Gastric Cancer Syndrome CDH1 Mutations and Beyond

Strike a balance between advanced breast cancer eradication and E-cadherin restoration: EMT events in the spotlight

Cancer cells often express a massive amount of proteins that are needed to their own proliferation.  One of the molecular abnormalities related to tumour progression, invasion and fixation requires the impairment of E-cadh expression, a tumour invasion suppressor protein. Epithelial‑mesenchymal transitions (EMT), is associated with the silencing of E-cad expression and further expression of EMT related molecules, such as Akt2 and Twist, crucial for progression of non-invasive into a malignant metastatic carcinomas, due to a polarity and adhesion loss between adjacent cells.