FAK suppresses antigen processing and presentation to promote immune evasion in pancreatic cancer

Pancreatic ductal adenocarcinoma (PDAC) is generally regarded as an immunologically ‘cold’ tumor type, devoid of CD8 T- cell infiltration and unresponsive to single- agent immunotherapy. Findings identify a novel role for focal adhesion kinase (FAK) in regulating the antigenicity of PDAC in favor of an antitumor T- cell response. This was not simply the consequence of increased antigen presentation, but rather an extensive reprogramming of the antigen repertoire mediated via regulation of the immunoproteasome. Therapies aimed at FAK degradation may unlock additional therapeutic benefit for the treatment of PDAC through increasing antigen diversity and promoting antigen presentation. To investigate whether FAK expression had any impact on the cancer cell response to IFNγ, microarray profiling of tumor cell- secreted proteins are used to measure the secretion of chemokines and cytokines of FAK- wt and FAK-/-cells in vitro treated with 10 ng/mL IFNγ.

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#Microarray #Immunotherapy #Pancreaticcancer #Chemokineandcytokine