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Abstract 2285: Co-expressed gene networks in CRC CMS1 subtype


 Colorectal cancer (CRC) is a heterogenous disease driven by dysregulated Wnt, Ras-Raf-MAPK, TGF-β, and PI3K-Akt signaling, which leads to an upregulation of proliferative and survival signals from the tumor microenvironment. Molecular and genomic alterations, immune signatures and gene mutations contribute to the progression of CRC. The consensus molecular subtype (CMS), an RNA-based classification system with four classes, is used to better understand CRC heterogeneity. CMS1 is the immunogenic subtype, enriched with MSI; CMS2-CMS3 has epithelial characteristics; and CMS4 is characterized by mesenchymal transitions associated gene expression. CMS1 tumors display immune infiltration, hypermethylation and microsatellite instability, and are known to have a poorer prognosis. We investigated gene signatures and associated coding mRNAs, which are co-expressed by CMS1 CRC. We acquired CRC primary tumor samples from The Cancer Genome Atlas (TCGA). CXCL13, CXCR5, IL10, PIK3R5, PIK3AP1, CCL19 and other co-expressed genes were identified to be positively correlated with CMS1. The canonical pathways and their upstream regulators of this co-expressed network were analyzed using Gene Ontology (GO). The co-expressed network associated with CMS1 was significantly and positively correlated with PI3K, WNT, ERK1 and ERK2 activation. This network was also positively correlated to right-sided tumors, microsatellite instability, chemokine-mediated signaling pathways, and immune responses. Our findings have confirmed and identified new gene signatures significantly correlated with CMS1, which in no doubt activate key pathways associated with CRC progression.
 Citation Format: Sha'Kayla K. Nunez, Corey D. Young, Ti'ara L. Griffen, Scott Kopetz, James W. Lillard. Co-expressed gene networks in CRC CMS1 subtype [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2285.