Cancer metastasis is accelerated through immunosuppression during Snail-induced EMT of cancer cells.

By C. Kudo-Saito, Hiromi Shirako, T. Takeuchi, Y. Kawakami. Cancer Cell, 2009

831 citations recorded by the source corpus.

Subfields: Biotechnology, Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/3860f3c7cf4e3dc43218b86b2721903c73c92afb

How researchers see this paper

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

In Biotechnology

1. J. P. Thiery
2. M. Nieto
3. R. Huang
4. R. Weinberg
5. X. Ye
6. Yibin Kang
7. Lisa M. Coussens

In Immunology

1. G. Dranoff
2. J. López-Novoa
3. M. Nieto
4. G. Freeman
5. R. Weinberg
6. D. Pardoll
7. Lieping Chen
8. E. Wherry

In Oncology

1. R. Weinberg
2. M. Nieto
3. J. P. Thiery
4. X. Ye
5. R. Huang
6. Yibin Kang
7. G. Dranoff
8. H. Acloque

Citations in the corpus

• The ins and outs of the epithelial to mesenchymal transition in health and disease. (2011, background): “As such, Snail has been associated with the activation of immunosuppressive cytokines as well as with regulatory T cells, resistance to cytotoxic T lymphocytes, and the generation of impaired dendritic cells (Kudo-Saito et al. 2009).”
• Epithelial-Mesenchymal Transition in Cancer: Parallels Between Normal Development and Tumor Progression (2010, background): “Tumor cells that have undergone EMT in response to forced expression of Snail induce immunosuppressive cytokines and impair tumor surveillance mechanisms [92].”
• The Role of Snail in EMT and Tumorigenesis (2013, background): “Knockdown of Snail significantly inhibits tumor growth and metastasis by increasing tumor-infiltrating lymphocytes and systemic immune responses [83].”
• Activation of the PD-1 pathway contributes to immune escape in EGFR-driven lung tumors (2013, background): “Previous reports have shown that these cytokines promote tumor growth and cause immune suppression (29-31) and, in the case of TGF-β, also support tumor metastasis by inducing epithelial to mesenchymal transition, which has been associated with resistance to cytotoxic T cell killing (32, 33).”
• Epithelial-mesenchymal transitions in development and disease. (2009, background): “Snail1 expression is correlated with breast tumor recurrence (Moody et al., 2005), and Snail is associated with the activation of immunosuppressive cytokines, regulatory T cells, cytotoxic T lymphocytes resistance, and the generation of impaired dendritic cells (Kudo-Saito et al., 2009).”
• Epithelial-Mesenchymal Transition in Cancer: A Historical Overview (2020, background): “In this context, an increased immunosuppressive regulatory T cells infiltration in tumor microenvironment when EMT is stimulated by Snail in melanoma cells was found [144].”
• Epithelial-mesenchymal plasticity in cancer progression and metastasis (2019, background): “In melanoma, SNAI1-induced EMT accelerates cancer metastasis partly through induction of regulatory T cell-mediated immunosuppression (Kudo-Saito et al., 2009).”
• 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 Plasticity: A central regulator of cancer progression (2015, background): “In melanoma, expression of the Snail EMT-TF can simultaneously inhibit differentiation of cytotoxic T cells and induce the formation of immunosuppressive regulatory T cells, the latter effect being mediated through production of thrombospondin (Kudo-Saito et al., 2009).”