Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Improvement of hepatocellular carcinoma using hepatocyte-derived liver progenitor-like cells (HepLPCs): therapeutic, proliferation arrest, malignant biological behavior changes，signal pathway screening

ABSTRACT: We employed a co-culture experiment and found that human hepatocyte-derived liver progenitor-like cells (HepLPCs) significantly inhibited the proliferation of hepatocellular carcinoma (HCC) in a specific manner and altered their malignant biological behavior without affecting cell aging, autophagy, apoptosis and so on. To evaluate the mechanism of action, HepG2 and Hep3B after co-cultured with HepLPCs gene profiling were performed, and we observed, in addition to proliferative blockade induction, that cascade events originated from mitochondrial dysfunction.

ORGANISM(S): Homo sapiens

PROVIDER: GSE256376 | GEO | 2025/05/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Improvement of hepatocellular carcinoma using hepatocyte-derived liver progenitor-like cells (HepLPCs): therapeutic, proliferation arrest, malignant biological behavior changes，signal pathway screening

Project description:Improvement of hepatocellular carcinoma using hepatocyte-derived liver progenitor-like cells (HepLPCs): therapeutic, proliferation arrest, malignant biological behavior changes，signal pathway screening

| PRJNA1079293 | ENA

Improvement of liver cirrhosis using hepatocyte-derived liver progenitor-like cells (HepLPCs): a prospective, open label, single arm, safety trial

Project description:The escalating demand for liver transplantation, coupled with the scarcity of donor organs and inherent transplantation risks, underscores the urgent need for innovative cirrhosis treatments. To address this, we have developed a protocol for transforming human primary hepatocytes into expandable Hepatocyte-Derived Liver Progenitor-Like Cells (HepLPCs). In animal models, these cells exhibited anti-fibrotic properties and facilitated liver regeneration. This study comprises a pre-clinical phase and an inaugural clinical trial involving nine cirrhosis patients to assess the feasibility and safety of HepLPC treatment. The HepLPCs infusion was well-tolerated, devoid of transfusion reactions or dose-limiting toxicities. Primary outcome measures, encompassing safety and feasibility, were successfully met. Notably, the results revealed enhanced liver function following HepLPCs infusion, indicating significant improvements in cirrhosis indicators over a 6-month observation period. These promising findings advocate for the therapeutic potential of HepLPCs as an innovative strategy for liver cirrhosis, warranting further exploration through clinical trials, particularly in decompensated cirrhosis and acute-on-chronic liver failure patients.

2024-12-30 | GSE248227 | GEO

Hepatocyte-derived liver progenitor-like cells attenuate liver cirrhosis via induction of apoptosis in hepatic stellate cells

Project description:Cell therapy shows great promise as an alternative therapy for the cirrhotic liver. We have previously developed an approach for efficient expansion of both murine and human hepatocyte-derived liver progenitor-like cells (HepLPCs) in vitro without genetic modification. The current study aimed to apply HepLPCs to treatment of liver cirrhosis. The effects of allogeneic HepLPCs transplantation were studied in rat models of liver cirrhosis induced by carbon tetrachloride (CCl4) . Liver tissues were collected and analyzed by RNA sequencing array to analyze changes in histology or gene expression patterns. Transplantation of HepLPCs reduced active fibrogenesis and net fibrosis in model of liver cirrhosis. Apoptosis of hepatic stellate cells (HSCs) was observed in vivo after HepLPCs treatment.

2024-04-10 | GSE200550 | GEO

Exosomal miR-183-5p from human hepatocyte-derived liver progenitor-like cells promotes liver regeneration during acute liver failure

Project description:Hepatocyte-derived liver progenitor-like cells (HepLPCs) can reversibly differentiate into mature hepatocytes and play important roles in liver regeneration following acute liver failure. However, the mechanisms by which HepLPCs exert these regulatory effects are unclear. Herein, we report that HepLPCs participate in reinitiating liver regeneration and improving survival during acute liver failure, at least in part, via miRNA-183-5p, which is released from HepLPCs in extracellular vesicles. Thus, these findings may identify novel targets and strategies for the treatment of acute liver failure.

2024-12-06 | GSE226645 | GEO

A single-cell RNA-Seq of human hepatocyte-derived liver progenitor-like cells

Project description:10X Genomics Single Cell Gene Expression was performed to comprehensively characterize cell subpopulations within human hepatocyte-derived liver progenitor-like cells (HepLPCs).

2018-06-22 | GSE116113 | GEO

Chemically Induced CD24+ hepatocyte-derived liver progenitor-like cells revert chronic hepatic dysfunction

Project description:Administration of soluble molecules to induce endogenous adult liver progenitor-like cells may provide a clinically and effectively applicable approach for liver damage repair. Here, we report that HGF in combination with a cocktail of small molecules Y-27632, A-83-01, and CHIR99021 (HACY), which we have previously defined to convert mature hepatocytes (MHs) to liver progenitor-like cells (HepLPCs) in vitro, could induce the replenishment of endogenous HepLPCs and relieve chronic liver dysfunction during persistent injury. The liver progenitor cells surface marker, CD24, was found to be highly expressed in HepLPCs in vitro. Similarly, injection of HACY into mice with carbon tetrachloride (CCL4) treatment also induced conversion of mature hepatocytes to CD24+ progenitor-like cells in vivo, leading to the attenuation of liver fibrosis. Compared to the liver progenitor cells (LPCs) derived from nonparenchymal cells, HACY-induced CD24+ HepLPCs retained an increased hepatic function by RNA sequencing analysis and could promote restoration of liver function by replacing CCL4-impaired liver cells during chronic hepatic damages. And CD24+ liver stem cells could also be observed in human liver fibrosis tissues and expanded in 3D hepatic spheroid in the present of HACY. Together, the results of our study indicated that injection of a cocktail of HACY might be a valuable multiple targets therapy for patients with chronic liver fibrotic pathologies.

2019-07-01 | GSE125095 | GEO

Pentamethylquercetin induces Hep3B liver cancer cell apoptosis and cell cycle arrest via the ERK/NF-κB signaling pathway

Project description:In this study, we investigated the biological roles and potential mechanisms of pentamethylquercetin (PMQ), a natural polymethyl flavones, against Hep3B liver cancer cells. Cell viability and growth curves were determined using the cell counting kit-8 (CCK-8) assay; flow cytometry was used to detect cell cycle and apoptosis; colony formation assay and JC-1 staining were used to detect cell proliferation and mitochondrial membrane potential changes, respectively. Transcriptome sequencing and western blotting were respectively used to investigate transcription and expression changes in Hep3B cells treated with PMQ. Treatment with 30 and 100 μM PMQ more significantly inhibited cell growth and proliferation in Hep3B cells than in HepG2 and LO2 cells. PMQ induced Hep3B cell cycle arrest and apoptosis by significantly reducing CDK4, CDK6, Cyclin D1, Cyclin E1, Cyclin B1 and Bcl-2 expression and increasing Bax, CDK1 and cleaved PARP levels. Transcriptomic profiles and western blotting results revealed that the MAPK and TNF signaling pathways may be involved in PMQ-induced Hep3B apoptosis.

2024-04-01 | GSE244233 | GEO

Exploring the roles of Notch inhibitors and STAT3 inhibitors in the regulation of liver cancer proliferation

Project description:We discovered that the inhibition of both the Notch and STAT3 signaling pathways effectively suppressed the proliferation of liver cancer cells, which aligns with the results obtained from co-culturing with human hepatocyte-derived liver progenitor-like cells (HepLPCs).

2025-05-30 | GSE256378 | GEO

Improvement of liver cirrhosis using hepatocyte-derived liver progenitor-like cells (HepLPCs): a prospective, open label, single arm, safety trial

Project description:Improvement of liver cirrhosis using hepatocyte-derived liver progenitor-like cells (HepLPCs): a prospective, open label, single arm, safety trial

| PRJNA1043052 | ENA

Improvement of hepatocyte engraftment by co-transplantation with pancreatic islets in hepatocyte transplantation.

Project description:Because of the fragility of isolated hepatocytes, extremely poor engraftment of transplanted hepatocytes remains a severe issue in hepatocyte transplantation. Therefore, improving hepatocyte engraftment is necessary to establish hepatocyte transplantation as a standard therapy. Since the pancreatic islets are known to have favorable autocrine effects, we hypothesized that the transplanted islets might influence not only the islets but also the nearby hepatocytes, subsequently promoting engraftment. We evaluated the effects of islet co-transplantation using an analbuminemic rat model (in vivo model). Furthermore, we established a mimicking in vitro model to investigate the underlying mechanisms. In an in vivo model, the hepatocyte engraftment was significantly improved only when the islets were co-transplanted to the nearby hepatocytes (p < 0.001). Moreover, the transplanted hepatocytes appeared to penetrate the renal parenchyma together with the co-transplanted islets. In an in vitro model, the viability of cultured hepatocytes was also improved by coculture with pancreatic islets. Of particular interest, the coculture supernatant alone could also exert beneficial effects comparable to islet coculture. Although insulin, VEGF, and GLP-1 were selected as candidate crucial factors using the Bio-Plex system, beneficial effects were partially counteracted by anti-insulin receptor antibodies. In conclusion, this study demonstrated that islet co-transplantation improves hepatocyte engraftment, most likely due to continuously secreted crucial factors, such as insulin, in combination with providing favorable circumstances for hepatocyte engraftment. Further refinements of this approach, especially regarding substitutes for islets, could be a promising strategy for improving the outcomes of hepatocyte transplantation.

| S-EPMC8048420 | biostudies-literature

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