Association of TIGIT and CD155 with KRAS, NRAS, BRAF, PIK3CA, and AKT Gene Mutations, MSI Status, and Cytokine Profiles in Colorectal Cancer
Błażej Ochman, Piotr Limanówka, Sylwia Mielcarska, Agnieszka Kula, Miriam Dawidowicz, Dorota Hudy, Monika Szrot, Jerzy Piecuch, Zenon Czuba, Dariusz Waniczek, Elżbieta Świętochowska
TL;DR
This study explores how TIGIT and CD155 proteins relate to genetic mutations and immune responses in colorectal cancer.
Contribution
The study identifies TIGIT's association with MSI and BRAF mutations, suggesting its role in immune activation in colorectal cancer.
Findings
TIGIT and CD155 proteins are elevated in CRC tumors compared to margins.
TIGIT levels correlate with MSI status and BRAF mutations, while CD155 does not show consistent mutation-dependent differences.
TIGIT-high tumors show interferon/inflammatory signatures, while CD155-high tumors show proliferation-related signatures.
Abstract
TIGIT and its ligand CD155 (PVR) are emerging immune checkpoints in colorectal cancer (CRC), but their associations with mutational subtypes and the tumor immune milieu remain unclear. We quantified TIGIT and CD155 proteins by ELISA in paired CRC tumors and matched surgical margins (n = 131) and evaluated associations with clinicopathological features, MSI status, and KRAS/NRAS/BRAF/PIK3CA/AKT1 mutations (n = 104). Both TIGIT and CD155 were significantly elevated in tumor tissue versus margins (p < 0.0001) and showed no association with TNM stage, clinical stage, grade, or tumor location. TIGIT levels were higher in MSI than MSS tumors and in BRAF-mutant compared to BRAF wild-type tumors, while CD155 expression showed no consistent MSI- or mutation-dependent differences. Cytokine profiling identified IFN-g as the only shared positive associate of TIGIT and CD155; CD155 additionally…
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Taxonomy
TopicsCancer Immunotherapy and Biomarkers · Immune Cell Function and Interaction · Cell Adhesion Molecules Research