Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Evaluation the targeted nanobubbles mediated LND against hepatocellular carcinoma by sonodynamic therapy with RNA-Seq

ABSTRACT: Evaluation the targeted nanobubbles mediated LND against hepatocellular carcinoma by sonodynamic therapy with RNA-Seq

PROVIDER: PRJNA721203 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14209013_1.fastq.gz	Fastqsanger.gz
	SRR14209013_2.fastq.gz	Fastqsanger.gz
	SRR14209014_1.fastq.gz	Fastqsanger.gz
	SRR14209014_2.fastq.gz	Fastqsanger.gz
	SRR14209015_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Evaluation the targeted nanobubbles mediated LND against hepatocellular carcinoma by sonodynamic therapy with RNA-Seq

Project description:Sonodynamic therapy is an important approach in the treatment of hepatocellular carcinoma. A novel targeted nanobubbles loaded with HMME and LND was structured as sensibilizer, characterized the properties, and studied therapeutic effect on hepatocellular carcinoma. Next-generation high throughput RNA sequencing (RNA-Seq) was performed to accurately analyze the differential expression of mRNAs and lncRNA targets in hepatocellular carcinoma after sonodynamic therapy.

2022-03-02 | GSE171857 | GEO

Lefamulin targets ILF3 to overcome targeted therapy resistance in hepatocellular carcinoma []

Project description:Lefamulin targets ILF3 to overcome targeted therapy resistance in hepatocellular carcinoma []

| PRJNA1063443 | ENA

Lefamulin targets ILF3 to overcome targeted therapy resistance in hepatocellular carcinoma

Project description:Lefamulin targets ILF3 to overcome targeted therapy resistance in hepatocellular carcinoma

| PRJNA1063444 | ENA

Lefamulin targets ILF3 to overcome targeted therapy resistance in hepatocellular carcinoma

Project description:Acquired resistance represents a critical clinical challenge to molecular targeted therapies such as tyrosine kinase inhibitors (TKIs) treatment in hepatocellular carcinoma (HCC). Therefore, it is urgent to explore new mechanisms and therapeutics that can overcome or delay resistance. Here, we identified a U.S. Food and Drug Administration (FDA)-approved pleuromutilin antibiotic that overcomes sorafenib resistance in HCC cell lines, cell line-derived xenograft (CDX) and hydrodynamic injection mouse models. We demonstrated that lefamulin targets and binds Interleukin Enhancer-binding Factor 3 (ILF3) to inhibit sorafenib-induced mitochondrial ribosomal protein L12 (MRPL12) upregulation. Mechanistically, lefamulin directly binds to Ala-99 of ILF3 and interferes with acetyltransferase general control non-depressible 5 (GCN5) and CREB binding protein (CBP) mediated acetylation of Lys-100, which disrupting the ILF3-mediated transcription of MRPL12 and subsequent mitochondrial biogenesis. Clinical data further confirmed that high ILF3 or MRPL12 expression was associated with poor survival and targeted therapy efficacy in HCC. Conclusively, our findings suggest that ILF3 is a potential therapeutic target for overcoming resistance to TKIs, and lefamulin may be a novel combination therapy strategy for HCC treatment with sorafenib and regorafenib.

2024-01-17 | GSE252988 | GEO

Lefamulin targets ILF3 to overcome targeted therapy resistance in hepatocellular carcinoma []

2024-01-17 | GSE252987 | GEO

CRISPR screens uncover protective effect of PSTK to targeted therapy induced ferroptosis in hepatocellular carcinoma

Project description:Hepatocellular carcinoma (HCC) is one of the most frequent malignancies with extremely poor prognosis. Clinical efficacies of existing targeted therapy strategies were not satisfied due to targeted therapy resistance. In this study, we performed a series of CRISPR/Cas9 screens to identify synthetic lethality genes to improve the clinical response of HCC. CRISPR loss-of-function genetic screens were performed to identify synthetic lethality genes of targeted therapies (Abemaciclib, Palbociclib, Sorafenib, Lenvatinib, Regorafenib and Erastin) in HCC cell lines. RNA-seq analysis were performed to clarify potential mechanism. We identified that inhibition of phosphoseryl-tRNA kinase (PSTK) sensitized HCC cells to targeted therapies. PSTK contributes to resistance of targeted therapy induced ferroptosis.

2022-03-23 | GSE182185 | GEO

Evaluation of ATAD2 as a potential target in hepatocellular carcinoma

Project description:Evaluation of ATAD2 as a potential target in hepatocellular carcinoma

| PRJNA737831 | ENA

Targeted therapy in hepatocellular carcinoma.

Project description:Hepatocellular carcinoma (HCC) is one of the commonest cancers worldwide, as well as a common cause of cancer-related death. HCC frequently occurs in the setting of a diseased cirrhotic liver and many patients present at an advanced stage of disease. Together with a poor functional status, this often precludes the use of systemic therapy, especially conventional cytotoxic drugs. Moreover, HCC is known to be a relatively chemo-refractory tumor. There have been many targeted drugs that have shown potential in the treatment of HCC. Many clinical trials have been carried out with many more in progress. They include trials evaluating a single targeted therapy alone, two or more targeted therapy in tandem or a combination of targeted therapy and conventional chemotherapy. In this article, we seek to review some of the more important trials examining the use of targeted therapy in HCC and to look into what the future holds in terms of targeted treatment of HCC.

| S-EPMC3170762 | biostudies-other

nitidine chloride against hepatocellular carcinoma dataset

Project description:proteomics dataset used to verify the mechanism of nitidine chloride against hepatocellular carcinoma

2021-08-11 | PXD027852 |

Alpelisib combination treatment as novel targeted therapy against hepatocellular carcinoma.

Project description:Hepatocellular carcinoma (HCC) is the sixth most common primary cancer with an unsatisfactory long-term survival. Gain of function mutations of PIK3CA occur in a subset of human HCC. Alpelisib, a selective PIK3CA inhibitor, has been approved by the FDA to treat PIK3CA mutant breast cancers. In this manuscript, we evaluated the therapeutic efficacy of alpelisib, either alone or in combination, for the treatment of HCC. We tested alpelisib in mouse HCC induced by hydrodynamic injection of c-Met/PIK3CA(H1047R) (c-Met/H1047R), c-Met/PIK3CA(E545K) (c-Met/E545K), and c-Met/sgPten gene combinations. Alpelisib slowed down the growth of c-Met/H1047R and c-Met/E545K HCC but was ineffective in c-Met/sgPten HCC. Mechanistically, alpelisib inhibited p-ERK and p-AKT in c-Met/H1047R and c-Met/E545K HCC progression but did not affect the mTOR pathway or genes involved in cell proliferation. In human HCC cell lines transfected with PIK3CA(H1047R), alpelisib synergized with the mTOR inhibitor MLN0128 or the CDK4/6 inhibitor palbociclib to suppress HCC cell growth. In c-Met/H1047R mice, alpelisib/MLN0128 or alpelisib/palbociclib combination therapy caused tumor regression. Our study demonstrates that alpelisib is effective for treating PIK3CA-mutated HCC by inhibiting MAPK and AKT cascades. Furthermore, combining alpelisib with mTOR or CDK4/6 inhibitors has a synergistic efficacy against PIK3CA-mutated HCC, providing novel opportunities for precision medicine against HCC.

| S-EPMC8501067 | 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