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Abstract
Despite the accumulating evidences of the significance of humoral cancer immunity, its molecular mechanisms have largely remained elusive. Here we show that B-cell repertoire sequencing of 102 clinical gastric cancers and molecular biological analyses unexpectedly reveal that the major humoral cancer antigens are not case-specific neo-antigens but are rather commonly identified as ribonucleoproteins (RNPs) in the focal adhesion complex. These common antigens are shared as autoantigens with multiple autoimmune diseases, suggesting a direct molecular link between cancer- and auto-immunity on the focal adhesion RNP complex. This complex is partially exposed to the outside of cancer cell surfaces, which directly evokes humoral immunity and enables functional bindings of antibodies to cancer cell surfaces in physiological conditions. These findings shed light on humoral cancer immunity in that it commonly targets cellular components fundamental for cytoskeletal integrity and cell movement, pointing to a novel modality of immunotherapy using humoral immunological reactions to cancers.
Highlights
Despite the accumulating evidences of the significance of humoral cancer immunity, its molecular mechanisms have largely remained elusive
It was found that higher wholegenomic mutation burdens, as defined in our previous study[10], had an apparent tendency to be correlated with lower B cell receptors (BCRs) entropy among various subtypes of
We found that focal adhesion-related RNP complexes are common major humoral antigens in tumor microenvironments (Fig. 7), most of which are common targets of autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), myasthenia gravis (MG), mass spectrometry (MS), primary biliary cirrhosis (PBC), and s syndrome (SS) (Table 1)
Summary
Despite the accumulating evidences of the significance of humoral cancer immunity, its molecular mechanisms have largely remained elusive. We show that B-cell repertoire sequencing of 102 clinical gastric cancers and molecular biological analyses unexpectedly reveal that the major humoral cancer antigens are not case-specific neo-antigens but are rather commonly identified as ribonucleoproteins (RNPs) in the focal adhesion complex. These common antigens are shared as autoantigens with multiple autoimmune diseases, suggesting a direct molecular link between cancer- and auto-immunity on the focal adhesion RNP complex. Our immunogenetic investigation of 102 cases of GC reveals previously unknown and intriguing common features of humoral antigens in tumor environments
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