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β-arrestin1 is involved in hepatocellular carcinogenesis via an inflammation-mediated Akt signal

ABSTRACT: Hepatocellular carcinoma (HCC), the main form of liver cancer, is the sixth most common cancer and the third most frequent cause of cancer death worldwide1. The exact mechanism of HCC initiation and development is still unclear, though inflammation has been shown to play a key role in this progression. Herein, we performed a gene expression assay to screen for alterative expression of genes among normal liver tissues, HCC tissues and its paracancer tissues with hepatitis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE67764 | GEO | 2015/04/11

SECONDARY ACCESSION(S): PRJNA280844

REPOSITORIES: GEO

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β-arrestin1 is involved in hepatocellular carcinogenesis via an inflammation-mediated Akt signal

Project description:Hepatocellular carcinoma (HCC), the main form of liver cancer, is the sixth most common cancer and the third most frequent cause of cancer death worldwide1. The exact mechanism of HCC initiation and development is still unclear, though inflammation has been shown to play a key role in this progression. Herein, we performed a gene expression assay to screen for alterative expression of genes among normal liver tissues, HCC tissues and its paracancer tissues with hepatitis. A gene assay to screen the expression of total RNA in liver tissues, including 3 normal liver tissues, 3 HCC paracancer specimens and 3 HCC samples with HBV-induced hepatitis. The normal liver samples were obtained from normal hepatic tissue in three hepatic hemangioma surgical operative patients, and three matched pairs of HCC and its paracancer tissues were respectively obtained from three HCC surgical operative patients without any chemotherapy and radiotherapy.

2015-04-11 | E-GEOD-67764 | biostudies-arrayexpress

Site-specific N-glycoproteomic analysis of Intrahepatic cholangiocarcinoma and Hepatocellular carcinoma

Project description:In this study,we performed integrated glycoproteomic and global proteomic analysis of tumor tissues of ICC and HCC to investigate the differences in site-specific glycosylation and proteins between ICC and HCC tumors. The paired paracancer tissue were also included as controls to determine the site-specific glycosylation changes in ICC and HCC tumors. The alteration extents in glycopeptide, global proteome, and normalized glycosylation in different sample groups were systematically compared.

2022-08-11 | PXD020277 | Pride

NOTCH/HES5 signaling exhibits distinct roles in MYC- and AKT-driven liver carcinogenesis

Project description:Notch signaling plays a pivotal role in liver development and aberrant Notch signaling may lead to hepatocellular (HCC) or cholangiocellular carcinoma (CCA) development. Using whole exome sequencing of 54 human HCC samples, we discovered 19 somatic missense mutations in 15 different Notch pathway genes affecting 24.6% (14 of 57) of patients. Prediction of functional impact of these Notch pathway mutations revealed HES5-R31G to have high relevance.

2019-10-31 | GSE121362 | GEO

Single-Cell Map of Diverse Immune Phenotypes in Liver Microenvironment

Project description:As hepatocellular carcinoma (HCC) is the most common type of liver cancer, ranks the sixth leading cause of cancer-related death worldwide (Bray, F., et al. 2018, CA Cancer J Clin 68: 394-424), it is imminent to uncover the regulatory mechanism of immune cells in the liver microenvironment. Here, we perform deep single-cell RNA sequencing on immune cells isolated from tumors of hepatocellular carcinoma patients and healthy liver from donors.

2023-07-22 | GSE155481 | GEO

m6A seq in prostate cancer cell lines

Project description:In order to reveal the biological role of m6A in prostate cancer, we conducted m6A-seq on two pairs of cancer/paracancer tissues.

2024-10-09 | GSE240669 | GEO

Study on Immune Escape Mechanism of Early Colorectal Cancer Cells

Project description:Interventions: Normal mucosa:Normal mucosa;Adenoma:Adenoma;Early colorectal cancer:Early colorectal cancer;Advanced cancer:Advanced cancer;Advanced cancer:Advanced cancer;Paracancer tissues :Paracancer tissues Primary outcome(s): Gender;Age;Location;HLA-A;Fas;CCR5;FasL;HLA-E Study Design: Cohort study

| 2669919 | ecrin-mdr-crc

miR-579-3p controls hepatocellular carcinoma formation by regulating the PI3K-AKT pathway in chronically inflamed liver (mRNA expression)

Project description:Background & Aims: Chronic liver inflammation causes continuous liver damage with progressive liver fibrosis and cirrhosis, which may eventually lead to hepatocellular carcinoma (HCC). Whereas, the ten-year incidence for HCC in cirrhotic patients is approximately 20%, many cirrhotic patients remain tumor-free for their entire lives. Therefore, we wanted to clarify the mechanisms defining the different outcomes of chronic liver inflammation. Methods: We designed a longitudinal study comparing the mRNA and miRNA expression profiles in matched non-tumoral liver tissue from patients developing HCC (n = 30) versus patients remaining tumor-free (n = 27). The liver parenchyma was analyzed before and after HCC development in the same patient. Cirrhotic patients remaining tumor-free within a similar time frame served as a control cohort. mRNA expression of genes associated with cancer development and miRNAs were examined by the nCounterNanostring technology. The role of the identified genes involved in HCC development was evaluated by immunohistochemistry and in vitro assays. Results: Comparison of the two cohorts revealed that liver tissue from patients developing HCC displayed activation of NF-B, Insulin receptor and PI3K-AKT pathways, in parallel with increased hepatocyte proliferation and damage. Furthermore, downregulation of miR-579-3p was found as an early step in HCC development. MiR-579-3p directly attenuated PIK3CA expression and consequently AKT and pAKT. In vitro analyses confirmed that miR-579-3p controlled cell proliferation, migration and colony formation. Conclusions: Liver tissues from patients developing HCC revealed a more severe damage to the parenchyma with elevated hepatocyte proliferation. Moreover, miR-579-3p was identified as a potential novel tumor suppressor regulating PI3K-AKT signalling at the early stages of HCC development.

2021-06-20 | GSE116044 | GEO

miR-579-3p controls hepatocellular carcinoma formation by regulating the PI3K-AKT pathway in chronically inflamed liver (miRNA expression)

2021-06-20 | GSE116043 | GEO

Hepatic transcriptomic changes during non-alcoholic steatohepatitis (NASH)-associated liver carcinogenesis in mice

Project description:Hepatocellular carcinoma (HCC), which accounts for 90% of all primary livers tumors, is the fourth most common cancer in the world. The development of HCC is a long-term and complex process, and uncovering the molecular mechanisms associated with HCC development is critical for the disease diagnosis, prevention, and treatment. Exploring these mechanisms using human HCC samples is desirable, but frequently impractical, with a number of limitations and shortcomings. The STAMTM (Stelic Institute & Co, Tokyo, Japan) mouse model of NASH-associated liver carcinogenesis is considered a useful and relevant model for investigating the molecular pathogenesis of NASH-derived HCC. This model resembles the human HCC development associated with progression from simple steatosis to NASH, fibrosis, and HCC. In the present study, by using high-throughput whole genome microarrays (SurePrint G3 Mouse Gene Expression v2, 8x60K; Agilent Technologies, Santa Clara, CA), we examined the transcriptomic profiles in the livers of STAMTM mice at different stages of liver carcinogenesis, including steatosis (6 week time interval), NASH (8 weeks), fibrotic stage (12 weeks), and in full-fledged HCC (20 weeks). The results of microarray analyses showed significant progressive changes in hepatic gene expression during the development of HCC. A total of 970, 1462, 2742, and 2857 of differentially expressed genes were identified in the livers at 6, 8, 12, and 20 weeks, respectively. Detailed analysis of these differentially expressed genes will benefit the understanding of the underlying mechanisms of non-alcoholic fatty liver disease-derived HCC. Transcriptomic profile in the liver of STAM mice at 6 weeks (steatosis; n=3), 8 weeks (steatohepatitis; n=3) 12 weeks (fibrosis; n=4) and 20 weeks (HCC-stage tumor tissue, n=4) weeks. Age-matched control samples were also analyzed.

2016-06-22 | E-GEOD-83596 | biostudies-arrayexpress

tRF&tiRNA sequencing of human PTC tissues and corresponding paracancer tissues

Project description:Purpose: To study the expression and potential significance of tRF and tiRNA in PTC (Papillary thyroid carcinoma) by sequencing tRF and tiRNA in PTC tissues and corresponding paracancer tissues of thyroid cancer patients. Methods: Four pairs of PTC tissues and paracancer tissues were collected. Small RNA sequencing was performed on Illumina NexSeq instrument. Results: If P ≤ 0.05, fold change > 1.5 as the cutoff, there were 27 up-regulated tRFs & tiRNAs and 20 down-regulated tRFs & tiRNAs. Conclusions: Among the differentially expressed tRFs & tiRNAs, tiRNA-1:34-Lys-CTT-2 and tRF-1:30-Gly-CCC-3 may be the potential novel regulatory factors.

2022-02-26 | GSE197438 | GEO

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