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Links from GEO DataSets

Items: 20

1.

Transcriptome Analysis of Huh7 cells Infected with Adenovirus Overexpression GSTZ1 or PCK1

(Submitter supplied) Purpose:To understand the change in cellular metabolism and function for the overxepression of GSTZ1 or PCK1 in hepatoma cells. Methods:Total RNAs of AdGFP- , AdGSTZ1-, or AdPCK1-infected Huh7 cells were extracted using TRIzol (Invitrogen), following the manufacturer’s instructions. RNA-seq and bioinformatic data analysis were performed by Shanghai Novel Bio Ltd. Briefly, strand-specific RNA-seq libraries were prepared using the Total RNA-seq (H/M/R) Library Prep Kit (Vazyme Biotech, Nanjing, China) and were sequenced on Ion Torrent Proton sequencing platform. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17303
9 Samples
Download data: TXT
Series
Accession:
GSE117822
ID:
200117822
2.

RRBS of PCK1 knockout in PLC/PRF/5

(Submitter supplied) RRBS analysis of Parental and PCK1 knockout groups of PLC/PRF/5 cells.
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: XLS
Series
Accession:
GSE221725
ID:
200221725
3.

Re-expression of fetal IGF2 as a target for hepatocellular carcinoma therapy

(Submitter supplied) Non-coding microRNAs (miRNAs) mainly regulate the expression of targeted genes by regulating mRNA degradation or repressing their protein translation. MiRNA microarray profiling was then performed on 218 human HCC tumors samples, 10 samples from adjacent cirrhotic non-tumoral tissue, 10 samples from healthy liver and 12 HCC cell lines. In this study we investigated which miRNAs were differentially expressed in HCC compared to cirrhotic non-tumoral tissue and healthy liver.
Organism:
synthetic construct; Homo sapiens
Type:
Non-coding RNA profiling by array
Platform:
GPL14613
250 Samples
Download data: CEL
Series
Accession:
GSE74618
ID:
200074618
4.

Aberrantly microRNA profiling in cancerous hepatocytes versus normal primary hepatocytes

(Submitter supplied) MicroRNAs is a rapidly expanding area expected to change the way in which diseases will be diagnosed, treated and monitored in the future. Hepatocellular carcinoma (HCC) shows a rising incidence with high mortality but lack of effective targeted therapies. We identified the aberrantly expressed miRNAs involved in HCC through the comparison of miRNA expression profiling in cancerous hepatocytes with that in normal primary human hepatocytes and found 37 dysregulated miRNAs in HCC. more...
Organism:
Homo sapiens
Type:
Non-coding RNA profiling by array
Platform:
GPL8227
11 Samples
Download data: TXT
Series
Accession:
GSE20077
ID:
200020077
5.

Isoginkgetin induces autophagic cell death in hepatocellular carcinoma [ChIP-seq 2]

(Submitter supplied) Purpose: Our previous studies have identified isoginkgetin as an inducer of autophagic cell death in hepatocellular carcinoma. We set out to analyze how isoginkgetin regulates the genome-wide enhancer activity in HepG2 cells. Methods: ChIP-seqs for H3K4me, H4K8ac, H3K27me3 and H3K9ac were performed in HepG2 followed by treatment with 20 μM isoginkgetin for 24 h. Conclusions: Isoginkgetin treatment reduces the expression of glucose transporters and inhibts SLC2A1 enhancer activity in HepG2 cells.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
10 Samples
Download data: BW
Series
Accession:
GSE202612
ID:
200202612
6.

Isoginkgetin induces autophagic cell death in hepatocellular carcinoma

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL20795 GPL11154
18 Samples
Download data: BW
Series
Accession:
GSE188535
ID:
200188535
7.

Isoginkgetin induces autophagic cell death in hepatocellular carcinoma [ChIP-Seq]

(Submitter supplied) Purpose: Our previous studies have identified isoginkgetin as an inducer of autophagic cell death in hepatocellular carcinoma. We set out to analyze how isoginkgetin regulates the genome-wide enhancer activity in HepG2 cells. Methods: ChIP-seq for H3K27ac was performed in HepG2 followed by treatment with 20 μM isoginkgetin for 24 h. Conclusions: Isoginkgetin treatment reduces the expression of glucose transporters and inhibts SLC2A1 enhancer activity in HepG2 cells.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20795
4 Samples
Download data: BW
Series
Accession:
GSE188534
ID:
200188534
8.

Isoginkgetin induces autophagic cell death in hepatocellular carcinoma [RNA-Seq]

(Submitter supplied) Purpose: Our previous studies have identified Isoginkgetin as an inducer of autophagic cell death in hepatocellular carcinoma. We set out to analyze how isoginkgetin regulates gene expression in HepG2 cells. Methods: RNA-seq was performed with two repetitions in HepG2 followed by treatment with DMSO and 20 μM Isoginkgetin for 24 h. Conclusions: Isoginkgetin treatment reduces the expression of glucose transporters in HepG2 cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20795
4 Samples
Download data: CSV
9.

Oncogenic Serine-Threonine Kinase Receptor Associated Protein Supports Hepatocellular Carcinoma Cell Growth by Enhancing Wnt/β-catenin Signaling

(Submitter supplied) Serine-threonine kinase receptor-associated protein (STRAP) is upregulated in breast, colorectal and lung cancers, promoting their growth. We identify the upregulation of STRAP in hepatocellular carcinomas. Elevated STRAP endows tumor cells with growth advantage by reprograming a variety of metabolic processes and signaling pathways critical for hepatocellular carcinoma progression. Especially, enhanced Wnt/β-catenin signaling is likely to be a major effector of its tumor-promoting role.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
12 Samples
Download data: XLSX
Series
Accession:
GSE101061
ID:
200101061
10.

Oncometabolite succinylacetone activates HIF-1α signaling and promotes angiogenesis in GSTZ1-deficient HCC

(Submitter supplied) We describe a unique regulation of the succinylacetone/PHD2/HIF-1α axis by a metabolic enzyme GSTZ1. The total RNA was isolated from HepG2 cells stably transfected with or without GSTZ1-KO and analyzed using RNA-seq. Our work demonstrates that GSTZ1-deficient promotes HCC angiogenesis through stabilizing HIF-1α due to succinylacetone accumulation. In addition, the combination of targeting HIF-1α and PD-L1 could limit tumorigenesis and progression for Gstz1-/-mice, thus providing a potential target for HCC therapy.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20795
6 Samples
Download data: TXT
Series
Accession:
GSE192760
ID:
200192760
11.

Molecular targeting of CSN5 in human hepatocellular carcinoma: a mechanism of therapeutic response

(Submitter supplied) Development of targeted therapy for hepatocellular carcinoma (HCC) remains a major challenge. We have recently identified an elevated expression of the fifth subunit of COP9 signalosome (CSN5) in early HCC as compared to dysplastic stage. In the present study, we explored the possibility of CSN5 being a potential therapeutic target for HCC. We demonstrate that CSN5 knockdown by small interfering (si) RNA caused a block in cell proliferation and cell cycle progression, and induced apoptosis of HCC cells in vitro. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5210
Platform:
GPL6883
16 Samples
Download data: TXT
Series
Accession:
GSE26485
ID:
200026485
12.
Full record GDS5210

CSN5 depletion effect on hepatocellular carcinoma cell lines

Analysis of Huh7 and HepG2 hepatocellular carcinoma (HCC) cells depleted for CSN5, the fifth subunit of the COP9 signalosome. CSN5 expression is elevated in early HCC. Result provide insight into the role of CSN5 in the pathogenesis of HCC.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 cell line, 2 protocol sets
Platform:
GPL6883
Series:
GSE26485
16 Samples
Download data
13.

T3 and Glucose Increase Expression of Phosphoenolpyruvate Carboxykinase (Pck1) Leading to Increased ß-Cell Proliferation

(Submitter supplied) Thyroid hormone (T3) and high glucose concentrations are critical components of β-cell maturation and function. In the present study, we asked whether T3 and glucose signaling pathways coordinately regulate transcription of genes important for β-cell function and proliferation
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
20 Samples
Download data: TXT
Series
Accession:
GSE218334
ID:
200218334
14.

TRIM21 knockout mouse livers show enhanced antioxidant capacity and decreased compensatory proliferation

(Submitter supplied) Acute response to diethylnitrosamine treatment in TRIM21 wild-type and knockout mice were compared and differentially expressed genes were inendified at 48 hours
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21493
12 Samples
Download data: TXT
Series
Accession:
GSE164369
ID:
200164369
15.

Expression data from mouse hepatocellular carcinomas developed in Axin1 hepatocyte deleted mice

(Submitter supplied) Mouse liver tumors (T) and non tumoral adjacent livers (NT) sorted from mice knock out for Axin1 gene specifically in the hepatocytes . 3 mice of the brother hood non deleted for Axin1 were used as controls (WT) We used microarrays to determine the differential expression between tumoral and non tumoral tissue.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL18802
16 Samples
Download data: CEL
Series
Accession:
GSE107374
ID:
200107374
16.

RNA Helicase DDX5, a Negative Regulator of Wnt Activation and Hepatocyte Reprogramming in Hepatitis B Virus-associated Hepatocellular Carcinoma

(Submitter supplied) We demonstrate that HBV infection induces expression of the proto-oncogenic miR17~92 and miR106b~25 clusters which target the downregulation of DDX5. Increased expression of these miRNAs is also detected in HBV-driven HCCs exhibiting reduced DDX5 mRNA. Stable DDX5 knockdown (DDX5KD) in HBV replicating hepatocytes increased viral replication, and resulted in hepatosphere formation, drug resistance, Wnt activation, and pluripotency gene expression. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
19 Samples
Download data: BED, BW, TXT
17.

Deletion of HDAC1 induces caspase-independent autophagic cell death and mitotic defect in Hep3B cells

(Submitter supplied) HDAC1 aberrantly over expressed in HCC and it was considered as an oncogene gene in HCC development. So we want to analyze in greater detail of the genes regulated by HDAC1 using microarray assay.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
2 Samples
Download data: TXT
Series
Accession:
GSE31358
ID:
200031358
18.

UNC50 prompts G1/S transition and proliferation in HCC through regulation of epidermal growth factor receptor trafficking

(Submitter supplied) Background: UNC50 has long been recognized as a Golgi apparatus protein in yeast, and is involved in nicotinic receptor trafficking in Caenorhabditis elegans, but little is known about UNC50 gene function in human biology despite it being conserved from yeast to high eukaryotes. Objectives: We investigated the relation between UNC50 and human hepatocellular carcinoma (HCC) and the potential mechanisms underlying HCC development. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL14550
4 Samples
Download data: TXT
Series
Accession:
GSE63322
ID:
200063322
19.

A 5:2 intermittent fasting regimen initiated in the active phase ameliorates NASH, fibrosis and blunts HCC development via hepatic PPARα and PCK1

(Submitter supplied) The role and molecular mechanisms of intermittent fasting (IF) in non-alcoholic steatohepatitis (NASH) and its transition to hepatocellular carcinoma (HCC) are unknown. Here, we identified that an IF 5:2 regimen (two non-consecutive days of food deprivation per week), initiated in the active phase of mice, prevents NASH development as well as ameliorates established NASH and fibrosis without affecting total calorie intake. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
39 Samples
Download data: TSV, TXT
Series
Accession:
GSE255356
ID:
200255356
20.

High frequency of β-catenin mutations in mouse HCCs induced by a non-genotoxic CAR agonist

(Submitter supplied) Activation of Wnt/β-catenin signaling is frequent in human and rodent hepatocarcinogenesis. Although in mice, the tumor promoting activity of agonists of constitutive androstane receptor (CAR) occurs via selection of carcinogen-initiated cells harbouring β-catenin mutations, the molecular alterations leading to hepatocellular carcinoma (HCC) development by The CAR agonist 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP), in the absence of genotoxic injury are unknown. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
22 Samples
Download data: TXT
Series
Accession:
GSE113708
ID:
200113708
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