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Tracking tumor cell direct interactome reveals a proliferating cell layer competition structure for CTRB1-driven epithelial-stromal defense against cancer

ABSTRACT: Purpose: To explore the molecular mechanism of CTRB1 boosts host endows cell fitness to outcompete tumor cells, RNA sequencing was performed to analyzeand compare the gene signatures of between HEK 293FTGFP and HEK 293FTCTRB1-GFP cells. Methods: Total mRNA was extracted from HEK 293FTGFP and HEK 293FTCTRB1-GFP cells. Then RNA quality was assessed using an Agilent Bioanalyzer 2100 and the sample reads were sequenced using Illumina NovaSeq 6000 platform. Results: Our results revealed differentially expressed genes in HEK 293FTCTRB1-GFP cells when compared with HEK 293FTGFP cells. Further KEGG analysis reveal that expression of CTRB1 influenced several proliferation-related signaling pathways, including Hippo-YAP, WNT, and Notch. Conclusion: Our study present the detailed transcripts analysis of HEK 293FTGFP and HEK 293FTCTRB1-GFP cells. Based on RNA-seq transcriptome characterization, indicating that CTRB1 can activate multiple proliferation-related signaling pathways expression to dictate cell fitness during cell competition.

ORGANISM(S): Homo sapiens

PROVIDER: GSE289634 | GEO | 2026/05/20

REPOSITORIES: GEO

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Project description:In early mammalian embryogenesis, the selective elimination of suboptimal cells is critical for developmental integrity. Cell competition is a non-autonomous quality control in which “winner” cells eliminate viable but suboptimal “loser” cells based on their relative difference in fitness. Due to its central role in fitness perception, loss of p53 results in the emergence of “supercompetitor” cells, which stand at the apex of cell competition and induce apoptosis in neighboring wild-type (WT) cells. Here, we investigate cell competition dynamics using mosaic 3D mouse gastruloids, an embryonic stem cell (ESC)-based in vitro model of gastrulation, composed of defined numbers of WT and p53-KO cells. In mosaic gastruloids, even low numbers of p53-KO cells robustly outcompete WT cells, and introduction of as few as two p53-KO cells is sufficient to measurably impair neighboring WT cell growth. Cell competition in gastruloids is independent of proliferation rates, nutrient availability, or reactive oxygen species, and not influenced by Nodal and ERK signaling. However, we observe that Wnt and BMP signaling protect from cell competition, which is exclusively driven by intrinsic apoptosis, as indicated by Bcl2-mediated complete rescue of WT cells. During gastruloid development, cell competition is temporally restricted to a window of 48–96 hours after aggregation, mirroring embryonic days E5.5–E7.5 in the mouse. Heterochronic mosaic gastruloid experiments demonstrate that relative differences in pluripotency levels are neither necessary nor sufficient to cause supercompetition, but that cell competition is contingent on both competitors residing within the developmental window permissive to competition. Neither pluripotent mosaic 3D aggregates, nor 3D EpiGastruloids, which model more advanced developmental processes, display any competition, supporting the hypothesis that developmental cell competition is specific to the onset of gastrulation. Our findings offer insights into the mechanisms of cell fitness evaluation in mammalian embryogenesis and establish gastruloids as a powerful 3D model for investigating developmental stage-specific cell competition.

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Tracking tumor cell direct interactome reveals a proliferating cell layer competition structure for CTRB1-driven epithelial-stromal defense against cancer

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