Effect of FOXA1 knockdown on gene expression in sulfasalazine-resistant OSC19SSZR cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE241108 | GEO | 2023/09/15
REPOSITORIES: GEO
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Project description:Effect of FOXA1 knockdown on gene expression in sulfasalazine-resistant OSC19SSZR cells
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Project description:Gene expression analysis of parental and sulfasalazine-resistant human oral squamous carcinoma cell line OSC19
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Project description:UIntroduction: Ulcerative colitis (UC) is a life-threatening heterogeneous condition characterized by inflammation of the colon. Endoplasmic reticulum aminopeptidase 1 (ERAP1) is essential for antigen processing and immune regulation, however, its specific role in UC pathogenesis and therapeutic response remains unclear. This study aimed to investigate the role of ERAP1 in the response to sulfasalazine, a standard treatment for UC, using an ERAP1-heterozygous (ERAP1+/-) mouse model susceptible to colitis. Methods: Wild-type (WT) and ERAP1+/- mice were treated with 2.5% dextran sulfate sodium to induce colitis, followed by sulfasalazine administration. Colitis severity was assessed through histopathology. Immune cell populations, including neutrophils, dendritic cells, T cells, and NK1.1+ cells, were analyzed using flow cytometry. RNA sequencing of colonic tissues was performed to assess gene expression changes associated with reduced ERAP1 expression. Results: ERAP1+/- mice exhibited mildly increased susceptibility to DSS-induced colitis, with greater weight loss and distinct alterations in immune cell infiltration compared to WT mice. These differences were further pronounced after sulfasalazine treatment. RNA sequencing identified 428 differentially expressed genes between ERAP1⁺/⁻ and WT mice. Among these, 28 genes were previously associated with colitis or colorectal cancer, of which 11 were upregulated and 17 downregulated in ERAP1+/- mice. RT-qPCR confirmed significantly elevated expression of Anxa9, Atp2a1, and Hepacam2 in ERAP1+/- mice after sulfasalazine treatment, indicating a differential therapeutic response. Conclusion: Collectively, our findings show that partial ERAP1 deficiency promotes immune dysregulation, alters the expression of inflammation-associated genes, and impairs sulfasalazine efficacy. Therefore, ERAP1 may serve as a key regulator in the pathogenesis of UC and a potential target for therapy.
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Project description:Common overexpressing genes were identified in all human oral squamous cell carcinoma tissues and/or cultured cells. Ten oral squamous cell carcinoma tissues and 10 human oral squamous cell carcinoma cell lines were analyzed. Three normal oral mucosa tissues and a human non-neoplastic keratinocyte cell lines were used as control samples.
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Project description:To analyze gene expression profiles of differentiated and undifferentiated cancer cells, oral squamous cell carcinoma cell line HSC-2 cells were cultured under normal or adhesion-restricted condition and subjected to cDNA microarray analysis.
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Project description:FOXA1 is an epithelial transcription factor that is often found dysregulated in prostate cancer. Previous studies have reported both tumor-promoting and -inhibitory functions of FOXA1. However, a comprehensive analysis of FOXA1 in a physiological, immune-competent setting is still lacking. We here report a novel genetically engineered mouse model with Foxa1 KO in the Pten-null prostate epithelium for the study of FOXA1 loss within an immune-competent prostate tumor context. Here, we report Foxa1 loss induces prostate cancer lineage switch from a luminal-like to a more aggressive basal/squamous-like phenotype, which is accompanied by inflammatory and immunosuppressive cytokine signaling. Mechanistically, in addition to inducing luminal genes, we found FOXA1 directly inhibits several basal/squamous, inflammatory, and cytokine genes, such that its loss unleashes their expression. Moreover, Foxa1 loss induces a striking remodeling of the prostate tumor immune microenvironment, leading to increased immunosuppressive myeloid accumulation and dysfunctional and spatially confined T cells. Altogether, we report critical roles for FOXA1 loss in inducing basal/squamous de-differentiation and an immunosuppressive microenvironment.
2026-02-21 | GSE313915 | GEO
Project description:FOXA1 is an epithelial transcription factor that is often found dysregulated in prostate cancer. Previous studies have reported both tumor-promoting and -inhibitory functions of FOXA1. However, a comprehensive analysis of FOXA1 in a physiological, immune-competent setting is still lacking. We here report a novel genetically engineered mouse model with Foxa1 KO in the Pten-null prostate epithelium for the study of FOXA1 loss within an immune-competent prostate tumor context. Here, we report Foxa1 loss induces prostate cancer lineage switch from a luminal-like to a more aggressive basal/squamous-like phenotype, which is accompanied by inflammatory and immunosuppressive cytokine signaling. Mechanistically, in addition to inducing luminal genes, we found FOXA1 directly inhibits several basal/squamous, inflammatory, and cytokine genes, such that its loss unleashes their expression. Moreover, Foxa1 loss induces a striking remodeling of the prostate tumor immune microenvironment, leading to increased immunosuppressive myeloid accumulation and dysfunctional and spatially confined T cells. Altogether, we report critical roles for FOXA1 loss in inducing basal/squamous de-differentiation and an immunosuppressive microenvironment.
2026-02-21 | GSE282724 | GEO
Project description:FOXA1 is an epithelial transcription factor that is often found dysregulated in prostate cancer. Previous studies have reported both tumor-promoting and -inhibitory functions of FOXA1. However, a comprehensive analysis of FOXA1 in a physiological, immune-competent setting is still lacking. We here report a novel genetically engineered mouse model with Foxa1 KO in the Pten-null prostate epithelium for the study of FOXA1 loss within an immune-competent prostate tumor context. Here, we report Foxa1 loss induces prostate cancer lineage switch from a luminal-like to a more aggressive basal/squamous-like phenotype, which is accompanied by inflammatory and immunosuppressive cytokine signaling. Mechanistically, in addition to inducing luminal genes, we found FOXA1 directly inhibits several basal/squamous, inflammatory, and cytokine genes, such that its loss unleashes their expression. Moreover, Foxa1 loss induces a striking remodeling of the prostate tumor immune microenvironment, leading to increased immunosuppressive myeloid accumulation and dysfunctional and spatially confined T cells. Altogether, we report critical roles for FOXA1 loss in inducing basal/squamous de-differentiation and an immunosuppressive microenvironment.
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