GATA4 silenced HUH6 hepatoblastoma cells
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ABSTRACT:
PROVIDER: PRJNA434561 | ENA |
REPOSITORIES: ENA
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Project description:The effects of GATA4 silencing on global gene expression in HUH6 hepatoblastoma cells was analyzed. Using microarray analysis we identified a set of genes that are downregulated or upregulated following silencing of GATA4 in HUH6 cell line.
2018-08-06 | GSE110788 | GEO
Project description:GATA4 is frequently epigenetically silenced in lung cancers. However, the impact of GATA4 inactivation on tumorigenesis and related therapeutic strategy remain to be determined. Through the genome-wide screening of tumor suppressing transcription factors, we demonstrate that GATA4 functions as an essential tumor suppressor in lung cancer in vitro and in vitro. Interestingly, ectopic GATA4 expression resulted in cellular senescence. Mechanistically, GATA4 up-regulates multiple miRNAs (miRNA-32, miRNA-301b, miR-320a, and miR-590) targeting TGFB2 mRNA and causes ensuing downregulation of WNT7B level to induce senescence. TGFBRI inhibitor synergizes with MEK1/2 inhibitor to promote lung cancer regression in Kras G12D/GATA4-/- mouse models. Decreased GATA4 level in clinical specimens negatively correlates with WNT7B or TGFB2 level and is significantly associated with poor prognosis.
2017-12-01 | GSE85002 | GEO
Project description:Hepatoblastoma is a primary malignant liver tumor in children, thought to arise from abnormal liver development during the fetal period. Approximately 90% of cases harbor activating mutations in CTNNB1, which encodes β-catenin, while other genetic mutations are rare. Recent studies have shown that CTNNB1 mutations are frequently accompanied by increased expression of the transcriptional coactivator YAP, which promotes cell proliferation and suppresses apoptosis. Based on these findings, we established a hepatoblastoma model by introducing active forms of CTNNB1 and YAP into human iPSC-derived hepatoblasts. Cells transduced with both genes showed distinct morphological changes and upregulation of CTNNB1, YAP, and their downstream target genes. RNA-seq followed by Gene Set Enrichment Analysis (GSEA) revealed that the gene expression profile of these cells closely matches that of hepatoblastoma patients. Utilizing this model, we identified Prostate-Associated Gene 4 (PAGE4) as a novel candidate gene involved in hepatoblastoma progression. Functional analysis in hepatoblastoma cell lines (Huh6, HepG2) demonstrated that PAGE4 plays a role in promoting cell proliferation and resistance to apoptosis. Since PAGE4 is a known cancer/testis antigen with tumor-specific expression, it has been recognized as a potential target in cancer therapy. Our findings indicate that PAGE4 represents a novel and promising therapeutic target for hepatoblastoma.
2025-10-17 | GSE296904 | GEO
Project description:RNA sequencing of LINC00958 silenced and LINC00958 non-silenced Ishikawa cells
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Project description:GATA4 is frequently epigenetically silenced in lung cancers. However, the impact of GATA4 inactivation on tumorigenesis and related therapeutic strategy remain to be determined. Through the genome-wide screening of tumor suppressing transcription factors, we demonstrate that GATA4 functions as an essential tumor suppressor in lung cancer in vitro and in vitro. Interestingly, ectopic GATA4 expression resulted in cellular senescence. Mechanistically, GATA4 up-regulates multiple miRNAs (miRNA-32, miRNA-301b, miR-320a, and miR-590) targeting TGFB2 mRNA and causes ensuing downregulation of WNT7B level to induce senescence. TGFBRI inhibitor synergizes with MEK1/2 inhibitor to promote lung cancer regression in Kras G12D/GATA4-/- mouse models. Decreased GATA4 level in clinical specimens negatively correlates with WNT7B or TGFB2 level and is significantly associated with poor prognosis.
2017-12-01 | GSE85001 | GEO
Project description:GATA4 is frequently epigenetically silenced in lung cancers. However, the impact of GATA4 inactivation on tumorigenesis and related therapeutic strategy remain to be determined. Through the genome-wide screening of tumor suppressing transcription factors, we demonstrate that GATA4 functions as an essential tumor suppressor in lung cancer in vitro and in vitro. Interestingly, ectopic GATA4 expression resulted in cellular senescence. Mechanistically, GATA4 up-regulates multiple miRNAs (miRNA-32, miRNA-301b, miR-320a, and miR-590) targeting TGFB2 mRNA and causes ensuing downregulation of WNT7B level to induce senescence. TGFBRI inhibitor synergizes with MEK1/2 inhibitor to promote lung cancer regression in Kras G12D/GATA4-/- mouse models. Decreased GATA4 level in clinical specimens negatively correlates with WNT7B or TGFB2 level and is significantly associated with poor prognosis.
2017-12-01 | GSE84852 | GEO
Project description:Hepatoblastoma is the most common primary liver malignancy in children, and outcomes remain poor for patients with metastatic disease. Long non-coding RNAs (lncRNAs) regulate tumor behavior, but their role in metastatic hepatoblastoma is not well defined. This study investigated the expression and functional significance of the lncRNA, maternally expressed gene 3 (MEG3), in a metastatic model of hepatoblastoma. RNA sequencing compared the metastatic hepatoblastoma cell line HLM_2 with its parental HuH6 cell line to identify differentially expressed lncRNAs. MEG3 expression was examined using hepatoblastoma patient datasets and validated using qPCR in cell lines, orthotopic tumors, and COA67 patient-derived xenografts. Functional effects of MEG3 knockdown in HLM_2 cells were evaluated with siRNA to evaluate clonogenicity, tumorsphere formation, migration, and invasion. The effects of MEG3 overexpression on clonogenicity, migration, and invasion were assessed in HuH6 cells. MEG3 was significantly upregulated in metastatic cells and orthotopic tumors compared with controls. MEG3 silencing reduced clonogenicity, tumorsphere formation, migration, and invasion. MEG3 overexpression increased clonogenicity, migration, and invasion. These findings indicate that MEG3 is upregulated in metastatic hepatoblastoma and may contribute to aggressive tumor phenotype, warranting further examination of the mechanistic role of MEG3 in hepatoblastoma, and its relevance as a biomarker or therapeutic target.
2026-03-04 | GSE316609 | GEO
Project description:The mechanisms underlying hepatoblastoma are not well defined. To address this, we generated transcriptomic profiles of normal, background, and hepatoblastoma liver samples from patients aged 0.01 months to 6 years, using RNA-sequencing. Hepatoblasoma was histologically confirmed. Here we focus on the elevation of stem cell markers and the loss of tumor suppressor proteins leading to the development of hepatoblastoma in very young children.
2018-07-01 | GSE81928 | GEO
Project description:RNAseq of DHX15-silenced endothelial cells
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