Sara Canato

ORCID: 0000-0002-1102-0192
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About
Contact & Profiles
Research Areas
  • Cystic Fibrosis Research Advances
  • Cancer-related gene regulation
  • Cancer Cells and Metastasis
  • Cellular Mechanics and Interactions
  • Cellular transport and secretion
  • RNA Interference and Gene Delivery
  • Cell death mechanisms and regulation
  • Wnt/β-catenin signaling in development and cancer
  • RNA Research and Splicing
  • Molecular Biology Techniques and Applications
  • Melanoma and MAPK Pathways
  • Genomics and Rare Diseases
  • Tissue Engineering and Regenerative Medicine
  • Hippo pathway signaling and YAP/TAZ
  • MicroRNA in disease regulation
  • Caveolin-1 and cellular processes
  • Neonatal Respiratory Health Research
  • Endoplasmic Reticulum Stress and Disease
  • Epigenetics and DNA Methylation
  • Immunotherapy and Immune Responses
  • Pancreatic function and diabetes
  • Pluripotent Stem Cells Research
  • Immune cells in cancer
  • Protein Degradation and Inhibitors
  • Hedgehog Signaling Pathway Studies

Champalimaud Foundation
2022-2024

i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto
2020-2023

Universidade do Porto
2020-2023

IPO Porto
2022-2023

Instituto Gulbenkian de Ciência
2019-2020

University of Lisbon
2013-2019

Istituti di Ricovero e Cura a Carattere Scientifico
2013

Abstract Epithelial-to-mesenchymal transition (EMT) has been associated with cancer cell heterogeneity, plasticity, and metastasis. However, the extrinsic signals supervising these phenotypic transitions remain elusive. To assess how selected microenvironmental control cancer-associated phenotypes along EMT continuum, we defined a logical model of cellular network that yields qualitative degrees adhesions by adherens junctions focal adhesions, two features affected during EMT. The attractors...

10.1158/0008-5472.can-19-3147 article EN Cancer Research 2020-03-26

Abstract Cystic fibrosis ( CF ), the most common recessive autosomal disease among Caucasians, is caused by mutations in gene encoding transmembrane conductance regulator CFTR ) protein. The mutation, F508del, leads to impaired plasma membrane trafficking. Therapies modulating basic defect are emerging, such as VX ‐809, a corrector of F508del‐ traffic which just succeeded Phase III clinical trial. We recently showed that ‐809 additive two other correctors VRT ‐325 and compound 4a). Here, we...

10.1002/prp2.152 article EN cc-by-nc-nd Pharmacology Research & Perspectives 2015-06-11

<div>Abstract<p>Stem cells (SC) and not progenitors (P) act as of origin basal cell carcinoma (BCC). The mechanisms promoting BCC formation in SCs or restricting tumor development Ps are currently unknown. In this study, we transcriptionally profiled found that <i>Survivin</i>, a pleiotropic factor promotes division inhibits apoptosis, was preferentially expressed SCs. Using genetic gain- loss-of-function mouse models, showed <i>Survivin</i> deletion...

10.1158/2159-8290.c.7662954 preprint EN 2025-02-07

ABSTRACT Alterations in the expression or function of cell adhesion molecules have been implicated all steps tumor progression. Among those, P-cadherin is highly enriched basal-like breast carcinomas, playing a central role cancer self-renewal, collective migration and invasion. To establish clinically relevant platform for functional exploration effectors vivo, we generated humanized Drosophila model. We report that actin nucleators, Mrtf Srf, are main fly. validated these findings human...

10.1242/dmm.049652 article EN cc-by Disease Models & Mechanisms 2023-02-01

The most common cystic fibrosis-causing mutation (F508del, present in ~85% of CF patients) leads to CFTR misfolding, which is recognized by the endoplasmic reticulum (ER) quality control (ERQC), resulting ER retention and early degradation. It known that exit from mediated specific retention/sorting signals include four arginine-framed tripeptide (AFT) motifs a diacidic (DAD) code controls interaction with COPII machinery. Here, we aim at obtaining global view protein interactors regulate...

10.3390/cells8040353 article EN cc-by Cells 2019-04-14

Abstract Aberrant expression of the Spectraplakin Dystonin (DST) has been observed in various cancers, including those breast. However, little is known about its role carcinogenesis. In this report, we demonstrate that a candidate tumour suppressor breast cancer and provide an underlying molecular mechanism. We show MCF10A cells, necessary to restrain cell growth, anchorage-independent self-renewal properties resistance doxorubicin. Strikingly, while maintains focal adhesion integrity,...

10.1038/s41598-019-56296-z article EN cc-by Scientific Reports 2019-12-27

Abstract Stem cells (SC) and not progenitors (P) act as of origin basal cell carcinoma (BCC). The mechanisms promoting BCC formation in SCs or restricting tumor development Ps are currently unknown. In this study, we transcriptionally profiled found that Survivin, a pleiotropic factor promotes division inhibits apoptosis, was preferentially expressed SCs. Using genetic gain- loss-of-function mouse models, showed Survivin deletion oncogene-expressing prevents formation. overexpression renders...

10.1158/2159-8290.cd-24-0263 article EN Cancer Discovery 2024-11-11

Abstract Tissue homeostasis relies on a precise balance of fate choices between renewal and differentiation, which is dysregulated during tumor initiation. Although much progress has been done over recent years to characterize the dynamics cellular at single cell level, their underlying mechanistic basis often remains unclear. In particular, although physical forces are increasingly characterized as regulators behaviors, unifying description how global tissue mechanics interplays with local...

10.1101/2024.12.12.628138 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-12-17

<div>Abstract<p>Epithelial-to-mesenchymal transition (EMT) has been associated with cancer cell heterogeneity, plasticity, and metastasis. However, the extrinsic signals supervising these phenotypic transitions remain elusive. To assess how selected microenvironmental control cancer-associated phenotypes along EMT continuum, we defined a logical model of cellular network that yields qualitative degrees adhesions by adherens junctions focal adhesions, two features affected during...

10.1158/0008-5472.c.6511966 preprint EN 2023-03-31

<div>Abstract<p>Epithelial-to-mesenchymal transition (EMT) has been associated with cancer cell heterogeneity, plasticity, and metastasis. However, the extrinsic signals supervising these phenotypic transitions remain elusive. To assess how selected microenvironmental control cancer-associated phenotypes along EMT continuum, we defined a logical model of cellular network that yields qualitative degrees adhesions by adherens junctions focal adhesions, two features affected during...

10.1158/0008-5472.c.6511966.v1 preprint EN 2023-03-31
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