Abstract :
[en] The LTalpha1beta2 and LIGHT TNF superfamily cytokines exert pleiotropic physiological functions through the activation of their cognate lymphotoxin-beta receptor (LTbetaR). Interestingly, since the discovery of these proteins, accumulating evidence has pinpointed a role for LTbetaR 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 LTbetaR signaling is also involved in diverse cell-intrinsic and microenvironment-dependent pro-oncogenic mechanisms, affecting several solid and hematological malignancies. Consequently, the usefulness of LTbetaR signaling axis blockade has been investigated as a potential therapeutic approach for cancer. Considering the seemingly opposite roles of LTbetaR signaling in diverse cancer types and their key implications for therapy, we here extensively review the different mechanisms by which LTbetaR activation affects carcinogenesis, focusing on the diverse contexts and different models assessed.
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