The Snail genes as inducers of cell movement and survival: implications in development and cancer

By Alejandro Barrallo-Gimeno, M. Nieto. Development, 2005

1,411 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/a5b836ed7754285d30c2d988228a48f36f76687b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

In Oncology

Citations in the corpus

Transcriptional regulation of cell polarity in EMT and cancer (2008, background): “To date, many different extracellular cues have been shown to trigger epithelial dedifferentiation and EMT, such as those involving transforming growth factor-b (TGF-b), Notch, fibroblast growth factor and Wnt signalling pathways (Barrallo-Gimeno and Nieto, 2005; De Craene et al., 2005a; Huber et al”
The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis (2022, background): “SNAIL1 and SNAIL2 have critical roles in the activation of the EMT program during embryonic development, fibrosis, and cancer [45].”
A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells (2008, background): “These include members of the Snail family, the basic helix–loop–helix family, Goosecoid and members of the ZFH family (zinc-finger E-box binding homeobox (ZEB)1 and ZEB2; Barrallo-Gimeno & Nieto, 2005; Hugo et al, 2007; Peinado et al, 2007).”
Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “cadherin repressors) have been found to be directly controlled by numerous extracellular signals and pathways [75,120,121].”
Visualizing stromal cell dynamics in different tumor microenvironments by spinning disk confocal microscopy (2008, background): “In addition to this, Snail1 is emerging as an overall regulator of EMT (Barrallo Gimeno and Nieto, 2005).”
The role of epithelial-mesenchymal transition in cancer pathology. (2007, background): “Snail decreases cell proliferation by favouring invasion versus tumour growth, and protects invading cells from apoptotic factors they could encounter during their migration through hostile territories.(14) Once arrived at the new sites, tumour cells would down-regulate Snail, and this would promote”
The many faces and functions of β‐catenin (2012, neutral): “Both of them repress E-cadherin transcription (Conacci-Sorrell et al , 2003; Barrallo-Gimeno and Nieto, 2005).”
TNF-α/NF-κB/Snail pathway in cancer cell migration and invasion (2010, background): “Snail was identified in Drosophila as a suppressor of the transcription of shotgun (an E-cadherin homologue) in the control of embryogenesis (Nieto, 2002; Barrallo-Gimeno and Nieto, 2005).”
Anoikis molecular pathways and its role in cancer progression. (2013, background): “the pro-apoptotic protein Bad, thus contributing to anoikis resistance [11].”
Complex networks orchestrate epithelial–mesenchymal transitions (2006, background): “The activation of signalling pathways also results in the activation of transcriptional regulators such as snail (now known as SNAI1 (Ref”
Inflammation and EMT: an alliance towards organ fibrosis and cancer progression (2009, background): “…as, in addition of triggering EMT, Snail-expressing cells are resistant to the cell death induced by the removal of survival factors, by genotoxic stress, chemotherapy and immunotherapy and even by TNF-a (reviewed in Barrallo-Gimeno & Nieto, 2005; see also Kudo-Saito et al, 2009; Vega et al, 2004).”
Epithelial-mesenchymal transitions: the importance of changing cell state in development and disease. (2009, neutral): “Once epithelial cells become competent to respond to EMT-inducing signals, these signals can promote disruption of the intercellular adhesion complexes and loss of the characteristic apico-basal polarity of the epithelial cells (3–5).”