Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Upregulation of the lncRNA MEG3 in Metastatic Hepatoblastoma

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE316609 | GEO | 2026/03/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

CRISPR/Cas9-mediated knockout of PIM3 suppresses tumorigenesis and cancer cell stemness in human hepatoblastoma cells.

Project description:Hepatoblastoma remains one of the most difficult childhood tumors to treat and is alarmingly understudied. Over half of patients initially present with locally advanced or metastatic disease and the prognosis for this cohort remains dismal. In addition, many of these children have disease that is resistant to standard therapies and will require novel and targeted therapies to effectively treat or manage their disease. We previously demonstrated that Proviral Insertion site in Maloney murine leukemia virus (PIM) kinases, specifically PIM3, are overexpressed in human hepatoblastoma cells and function to promote tumorigenesis. We aimed to use CRISPR/Cas9 gene editing technology with dual gRNAs to introduce large inactivating deletions in the PIM3 gene and achieve stable PIM3 knockout (KO) in the human hepatoblastoma cell line, HuH6. PIM3 KO of hepatoblastoma cells led to significantly decreased proliferation, viability, and motility, inhibited cell-cycle progression, decreased tumor growth in a xenograft murine model, and increased animal survival. Analysis of RNA sequencing data revealed that PIM3 KO downregulated expression of pro-migratory and pro-invasive genes and upregulated expression of genes involved in apoptosis and differentiation. Furthermore, PIM3 KO decreased hepatoblastoma cancer cell stemness as evidenced by decreased tumorsphere formation, decreased mRNA abundance of stemness markers, and decreased cell surface expression of CD133, a marker of hepatoblastoma stem cell-like cancer cells. Reintroduction of PIM3 into PIM3 KO cells rescued the malignant phenotype. These findings emphasize the role of PIM3 in promoting hepatoblastoma tumorigenesis and provide evidence that targeting PIM3 may offer a novel therapeutic approach for children with hepatoblastoma.

2021-10-27 | GSE164082 | GEO

GATA4 silenced HUH6 hepatoblastoma cells

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

GATA4 silenced HUH6 hepatoblastoma cells

Project description:GATA4 silenced HUH6 hepatoblastoma cells

| PRJNA434561 | ENA

A novel rexinoid agonist, UAB116, decreases metastatic phenotype in hepatoblastoma by inhibiting the Wnt/β-catenin pathway via upregulation of TRIM29

Project description:Hepatoblastoma (HB) is the most common pediatric primary liver tumor. About 20% of children have pulmonary metastasis at presentation. Survival rates for these children are dismal, not exceeding 25%. To study this subset of the HB population, we sequenced a metastatic HB cell line, HLM_2, and identified a downregulation in the liver X receptor (LXR)/rexinoid X receptor (RXR) pathway. LXR/RXRs are transcriptional regulators of genes involved in HB carcinogenesis including the Wnt/β-catenin signaling pathway. We assessed the effects of a novel LXR/RXR agonist, UAB116, on metastatic HB, hypothesizing that this compound would affect genes governing the Wnt/β-catenin pathway, leading to decreased metastatic phenotype in HLM_2 metastatic HB cells. We evaluated the effects on viability, proliferation, stemness, clonogenicity, and motility, and performed RNA sequencing to study differential gene regulation. Treatment with UAB116 (0-50 µM) for 72 hours decreased HLM_2 proliferation, stemness, clonogenicity, and invasion. RNA sequencing identified an 8-fold increase in TRIM29, a gene known to inhibit β-catenin, in cells treated with UAB116. These results show that treatment with an LXR/RXR agonist, UAB116, decreases metastatic HB cell proliferation, stemness, and invasion, likely through upregulation of TRIM29, a known regulator of the Wnt/β-catenin pathway, providing support for further exploration of LXR/RXR agonism as a therapeutic strategy for metastatic HB.

2025-05-22 | GSE290638 | GEO

UBE2C expression is elevated in hepatoblastoma and correlates with inferior patient survival

Project description:To gain insight into the pathobiology of hepatoblastoma (HB), RNA sequence analysis and protein-protein interaction analysis of previously established and sequenced HB samples were conducted. Ubiquitination was identified as a key pathway dysregulated in HB and UBE2C, encoding an E2 ubiquitin ligase often overexpressed in cancer cells, was markedly upregulated in 5 of the 6 HB cell lines. The silencing of UBE2C in HUH6 HB cell model resulted in decreased cell viability and migration. RNA sequencing analysis showed alterations in cell cycle regulation after UBE2C knockdown.

2023-04-30 | GSE201996 | GEO

Impact of SLC-0111 (U-104) on HUH6 hepatoblastoma cell transcriptome in normoxic and hypoxic conditions

Project description:Carbonic anhydrase 9 (CAIX) is a transmembrane metalloenzyme whose main function is to maintain the acid-base balance of the cell and hypoxic condition induces its expression. Solid tumors often exhibit regions with low oxygen content in areas where the blood supply is insufficient. CAIX is overexpressed in multiple solid tumors, including hepatoblastoma, the most frequent childhood liver malignancy. SLC-0111 is a commercially available CAIX inhibitor that is currently passed Phase I clinical trial on solid tumors. In this study we assessed the impact of SLC-0111 on transcriptomic changes of HUH6 hepatoblastoma cell line cells in both normoxic and hypoxic condition.

2022-04-30 | GSE185937 | GEO

Long non-coding RNAs and mRNAs in nasopharyngeal carcinoma metastasis

Project description:Increasing evidence has demonstrated a significant role for long non-coding RNAs (lncRNAs) in tumorigenesis. However, their functions in nasopharyngeal carcinoma (NPC) metastasis remain largely unknown. In this study, a model compared high and low metastatic NPC cell lines (5-8F vs. 6-10B and S18 vs. S26)was constructed to determine the expression profile of lncRNAs using the microarray analysis, and we found 167 lncRNAs and 209 mRNAs were differentially expressed. Validationof 26 significantly dysregulated lncRNAs by qRT-PCR showed the expression patterns of 22 lncRNAs were in accordance with the microarray data. Furthermore, the expression level of ENST00000470135, which was the most upregulated lncRNA in high metastatic cell lines, was significantly higher in NPC cell lines and tissues with lymph node metastasis（LNM）and knocking down ENST00000470135 suppressed the migration, invasion and proliferation of NPC cells in vitro. In conclusion, our study revealed expression patterns of lncRNAs in NPC metastasis. The dysregulated lncRNAs may act as novel biomarkers and therapeutic targets for NPC.

2017-02-22 | GSE89804 | GEO

PAGE4, upregulated in a novel iPSC-derived hepatoblastoma model, promotes hepatoblastoma progression

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

Secretome identification of immune cell factors mediating metastatic cell homing

Project description:Metastatic cell homing is a complex process mediated in part by diffusible factors secreted from immune cells found at a pre-metastatic niche. We report on connecting together secretomics and a TRanscriptional Activity CEll aRray (TRACER) to identify functional paracrine interactions between immune cells and metastatic cells as novel mediators of metastatic cell homing. Splenocytes from orthotopic mouse models of breast cancer were isolated to generate a diseased splenocyte conditioned media (D-SCM) containing immune cell secreted factors. MDA-MB-231 metastatic cell activity including cell invasion, migration, transendothelial migration, and proliferation were increased when cultured with D-SCM compared to healthy SCM (H-SCM) and unconditioned media controls. Our secretome analysis of D-SCM yielded secreted factor candidates that contribute to increased metastatic cell activity. In parallel, we identified active TFs within metastatic cells in response to the secreted factors using TRACER. We connected both data sets using MetaCore software to determine interactions between immune cell secreted factors and active metastatic cell TFs to narrow down functional secreted factor candidates that mediate metastatic cell homing. Haptoglobin was among the list of secreted factors and was validated in vitro as a key mediator of metastatic cell recruitment. Furthermore, we designed an implantable poly(lactide-co-glycolide) biomaterial scaffold as a mimic of the pre-metastatic niche to slowly release haptoglobin and demonstrate increased homing of metastatic cells to the scaffold in vivo. Taken together, our studies demonstrate a novel systems biology technique to identify functional paracrine signaling factors, which were validated to reveal mediators of metastatic cell homing.

2015-12-17 | PXD002051 | Pride

Invasion and metastasis related long non-coding RNA expression profiles in hepatocellular carcinoma

Project description:Aberrant expression of LncRNAs might be responsible for the HCC invasion and metastasis. we employed the LncRNAs microarray technology to study the LncRNAs expression profiles at genome-wide in hepatocellular carcinoma (HCC)tissue samples with early recurrence (less than 1 year, with invasion and metastasis out of liver) and late recurrence (longer than 2 years, without invasion and metastasis out of liver), which had different recurrent/metastatic potentials, by using normal liver tissue as control to screen the dysregulated LncRNAs which are potentially involved in the recurrence, invasion and metastasis process of HCC

2015-03-26 | GSE67260 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data