IL-1R signaling drives enteric glia-macrophage interaction in colorectal cancer progression [bulkRNA-Seq]

To examine the mechanisms by which EGCs affect the immune CRC compartment with particular regard to the TAMs, we first investigated their transcriptional adaptations upon CRC onset. To this end, we established an in vitro setup to study EGC-CRC interactions able to mimic the response of EGCs to the factors secreted by the TME. These EGCs, from now onwards defined as TME-conditioned medium-treated EGCs (TME-CM EGCs), were generated by stimulating primary EGCs with the CM of digested murine MC38 orthotopic tumor tissues (Figure 2A). Bulk RNA sequencing (RNA-seq) was performed to determine transcriptional differences in TME-CM EGCs, compared to unstimulated and healthy conditioned medium-treated (H-CM) primary EGCs, at different time points. Transcriptome analysis of in vitro primary neurosphere-derived embryonic EGCs alone or stimulated with healthy conditioned medium (H-CM) or tumor microenvironment conditioned medium (TME-CM) at different time points (6h, 12h, and 24h, n = 4).