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Comment
. 2016 Jul 15;22(14):3422-4.
doi: 10.1158/1078-0432.CCR-16-0336. Epub 2016 Apr 13.

Epithelial-Mesenchymal Transition and Immune Evasion during Lung Cancer Progression: The Chicken or the Egg?

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Comment

Epithelial-Mesenchymal Transition and Immune Evasion during Lung Cancer Progression: The Chicken or the Egg?

Ila Datar et al. Clin Cancer Res. .

Abstract

Epithelial-mesenchymal transition (EMT) is a complex process involved in metastasis. Immune evasion is required for tumor progression and is characterized by an ineffective antitumor immune response and upregulation of immune-suppressive signals. The coexistence of EMT and adaptive immune evasion opens the possibility of a mechanistic link between these processes. Clin Cancer Res; 22(14); 3422-4. ©2016 AACRSee related article by Lou et al., p. 3630.

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Figure 1
Figure 1. Possible association between EMT and anti-tumor immune response during (epithelial) cancer progression
Although EMT and tumor immune rejection/evasion are continuous, heterogeneous and potentially reversible processes, they frequently co-exist in lung adenocarcinomas suggesting a mechanistic link between them. Key EMT-mediators such as Snail, Twist, Zeb and aberrant β-catenin signaling can induce immune suppressive features in tumors. However, diverse inflammatory mediators such as TGF-β, TNF-α, IL-6, IL-8 and IL-10 or immune suppressive cells can promote an EMT-program in carcinoma cells. APC, antigen-presenting cell.

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References

    1. Lou Y, Diao L, Parra Cuentas ER, Denning WL, Chen L, Fan Y, et al. Epithelial-mesenchymal transition is associated with a distinct tumor microenvironment including elevation of inflammatory signals and multiple immune checkpoints in lung adenocarcinoma. Clin Cancer Res. 2016 Feb 5; Epub ahead of print. - PMC - PubMed
    1. Alsuliman A, Colak D, Al-Harazi O, Fitwi H, Tulbah A, Al-Tweigeri T, et al. Bidirectional crosstalk between PD-L1 expression and epithelial to mesenchymal transition: significance in claudinlow breast cancer cells. Mol Cancer. 2015;14:149. - PMC - PubMed
    1. Pietila M, Ivaska J, Mani SA. Whom to blame for metastasis, the epithelial-mesenchymal transition or the tumor microenvironment? Cancer Lett. 2016 Jan 11; Epub ahead of print. - PubMed
    1. Zheng H, Kang Y. Multilayer control of the EMT master regulators. Oncogene. 2014;33:1755–63. - PubMed
    1. Kudo-Saito C, Shirako H, Takeuchi T, Kawakami Y. Cancer metastasis is accelerated through immunosuppression during Snail-induced EMT of cancer cells. Cancer Cell. 2009;15:195–206. - PubMed

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