Context-dependent roles for lymphotoxin-β receptor signaling in cancer development

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Context-dependent roles for lymphotoxin-β receptor signaling in cancer development

Monday, 28.03.2016


Mónica T. Fernandes 1,2, Emmanuel Dejardin 3 and Nuno R. dos Santos 1,4,5

1 Centre for Biomedical Research (CBMR), University of Algarve, 8005-139 Faro, Portugal;

2 PhD Program in Biomedical Sciences, Department of Biomedical Sciences and Medicine, University of Algarve, 8005-139 Faro, Portugal;

3 Laboratory of Molecular Immunology and Signal Transduction, GIGA-Research, Molecular Biology of Diseases, University of Liège, 4000 Liège, Belgium;

4 Instituto de Investigação e Inovação em Saúde (I3S), Universidade do Porto, 4200 Porto, Portugal;

5 Institute of Pathology and Molecular Immunology of the University of Porto (IPATIMUP), 4200 Porto, Portugal.


The LTα1β2 and LIGHT TNF superfamily cytokines exert pleiotropic physiological functions through activation of their cognate lymphotoxin-β receptor (LTβR). Interestingly, since the discovery of these proteins accumulating evidence has pinpointed a role for LTβR signaling in carcinogenesis. Early studies have shown a potential anti-tumoral role in a subset of solid cancers either by triggering apoptosis in malignant cells or by eliciting an anti-tumor immune response. However, more recent studies provided robust evidence that LTβR signaling is also involved in diverse cell-intrinsic and microenvironment-dependent pro-oncogenic mechanisms, affecting several solid and hematological malignancies. Consequently, the usefulness of LTβR signaling axis blockade has been investigated as a potential therapeutic approach for cancer. Considering the seemingly opposite roles of LTβR signaling in diverse cancer types and their key implications for therapy, we here extensively review the different mechanisms by which LTβR activation affects carcinogenesis, focusing on the diverse contexts and different models assessed.


Biochimica et Biophysica Acta - Reviews on Cancer

http://authors.elsevier.com/a/1Sid2_,iJ7zVB5