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Gene expression profiles of cells from PDOs of normal colon and colorectal cancers [RNA-Seq]

ABSTRACT: Phenotypic plasticity is a hallmark feature driving cancer progression, metastasis, and therapy resistance. Fetal-like transcriptional programs have been increasingly implicated in promoting plastic cell states, yet their roles remain difficult to study due to limitations of existing culture models. Here, we establish a chemically defined patient-derived organoid (PDO) system that enables long-term expansion of colorectal cancer (CRC) cells while preserving fetal-like features associated with phenotypic plasticity. Using this model, we identify an oncofetal-like state (OnFS) that is enriched in advanced tumors and linked to key features of plasticity, including epithelial-mesenchymal plasticity, as well as increased metastasis and treatment resistance. Mechanistically, we show that FGF2–AP-1 signaling maintains the OnFS program and associated phenotypic plasticity in CRC. This model offers a powerful platform for studying the fetal-like features underlying cancer cell plasticity and their role in tumor progression and treatment resistance in CRC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE261004 | GEO | 2024/04/17

REPOSITORIES: GEO

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Single-cell gene expression profiles of cells from colorectal cancer and chemically induced PDOs [scRNA-Seq]

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