WNT Signaling in Cancer Immunosurveillance

Lorenzo Galluzzi; Stefani Spranger; Elaine Fuchs; Alejandro López-Soto

doi:10.1016/j.tcb.2018.08.005

WNT Signaling in Cancer Immunosurveillance

Trends Cell Biol. 2019 Jan;29(1):44-65. doi: 10.1016/j.tcb.2018.08.005. Epub 2018 Sep 13.

Authors

Lorenzo Galluzzi¹, Stefani Spranger², Elaine Fuchs³, Alejandro López-Soto⁴

Affiliations

¹ Department of Radiation Oncology, Weill Cornell Medical College, New York, NY 10065, USA; Sandra and Edward Meyer Cancer Center, New York, NY 10065, USA; Université Paris Descartes/Paris V, 75006 Paris, France. Electronic address: deadoc@vodafone.it.
² The Koch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA 02139, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
³ Robin Chemers Neustein Laboratory of Mammalian Cell Biology and Development, The Rockefeller University, New York, NY 10065, USA; Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
⁴ Departamento de Biología Funcional, Área de Inmunología, Universidad de Oviedo. Instituto Universitario de Oncología del Principado de Asturias (IUOPA), 33006 Oviedo, Spain; Instituto de Investigación Sanitaria del Principado de Asturias (IISPA), 33011 Oviedo, Asturias, Spain. Electronic address: lopezsalejandro@uniovi.es.

Abstract

Deregulated WNT signaling has been shown to favor malignant transformation, tumor progression, and resistance to conventional cancer therapy in a variety of preclinical and clinical settings. Accumulating evidence suggests that aberrant WNT signaling may also subvert cancer immunosurveillance, hence promoting immunoevasion and resistance to multiple immunotherapeutics, including immune checkpoint blockers. Here, we discuss the molecular and cellular mechanisms through which WNT signaling influences cancer immunosurveillance and present potential therapeutic avenues to harness currently available WNT modulators for cancer immunotherapy.

Keywords: BRAF; CTLA4; GSK3; PD-L1/PD-1 axis; cancer immunotherapy; tumor microenvironment; β-catenin.

Publication types

Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review

MeSH terms

Humans
Immunologic Surveillance / immunology*
Immunotherapy*
Neoplasms / immunology*
Neoplasms / therapy*
Wnt Proteins / metabolism*
Wnt Signaling Pathway / immunology*

Substances

Wnt Proteins

Abstract

Publication types

MeSH terms

Substances

Grants and funding