Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data of tigecycline-treated liver cancer cells

ABSTRACT: Expression data of tigecycline-treated liver cancer cells

PROVIDER: PRJNA821687 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18555112_1.fastq.gz	Fastqsanger.gz
	SRR18555112_2.fastq.gz	Fastqsanger.gz
	SRR18555113_1.fastq.gz	Fastqsanger.gz
	SRR18555113_2.fastq.gz	Fastqsanger.gz
	SRR18555114_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Expression data of tigecycline-treated liver cancer cells

Project description:Treatment of advanced liver cancer still faces great challenges. Identification of tumor dependencies is important for developing novel therapeutic strategies for liver cancer. Here, we identified mitochondrial translation as a major vulnerability of liver cancer by genome-wide CRISPR screen. Targeting mitochondrial translation by tigecycline showed therapeutic potential in liver cancer. While some liver cancer cells were extremely insensitive to tigecycline.Thus,RNA sequencing was performed to explore mechanisms.

2022-04-26 | GSE199842 | GEO

Mechanism of abnormal coagulation induced by tigecycline in cancers

Project description:Tigecycline is a broad-spectrum active intravenous antibiotic that is also active against methicillin-resistant staphylococcus aureus. In Phase 3 and 4 clinical trials, increased all-cause mortality was observed in patients treated with tigecycline compared to patients in the control group. The reason for the increase is not yet clear. In this study, we found tigecycline could cause abnormal coagulation in tumor patients, especially in patients with hematological malignancies. The main manifestations were decreased fibrinogen and prolonged activated prothrombin time (APTT), thrombin time (TT) and D-dimer. In addition, functional studies have found that tigecycline could inhibit platelet adhesion and aggregation, and the patient's coagulation function could gradually recover after discontinuation. Gene sequencing results suggested that tigecycline could significantly regulate the expression of genes related to platelet function pathways, and could increase the incidence of single nucleotide polymorphisms and the number of alternative splices in CHO cells with tigecycline treatment. Abnormal platelet function and low numbers are common in patients with hematological malignancies. Our study could explain the mechanism of abnormal coagulation caused by tigecycline. At the same time, a warning should be given when doctors applied tigecycline to cure infections in tumor patients.

2022-06-01 | GSE198830 | GEO

The Transcriptomic Signature of Tigecycline in Acinetobacter baumannii

Project description:Tigecycline, a protein translation inhibitor, is a treatment of last resort for infections caused by the opportunistic multidrug resistant human pathogen Acinetobacter baumannii. However, strains resistant to tigecycline were reported not long after its clinical introduction. Translation inhibitor antibiotics perturb ribosome function and induce the reduction of (p)ppGpp, an alarmone involved in the stringent response that negatively modulates ribosome production. Through RNA sequencing, this study revealed a significant reduction in the transcription of genes in citric acid cycle and cell respiration, suggesting tigecycline inhibits or slows down bacterial growth. Our results indicated that the drug-induced reduction of (p)ppGpp level promoted the production but diminished the degradation of ribosomes, which mitigates the translational inhibition effect by tigecycline. The reduction of (p)ppGpp also led to a decrease of transcription coupled nucleotide excision repair which likely increases the chances of development of tigecycline resistant mutants. Increased expression of genes linked to horizontal gene transfer were also observed. The most upregulated gene, rtcB, involving in RNA repair, is either a direct tigecycline stress response or is in response to the transcription de-repression of a toxin-antitoxin system. The most down-regulated genes encode two b-lactamases, which is a possible by-product of tigecycline-induced reduction in transcription of genes associated with peptidoglycan biogenesis. This transcriptomics study provides a global genetic view of why A. baumannii is able to rapidly develop tigecycline resistance.

2020-08-03 | GSE131451 | GEO

Expression data from sulfisoxazole-treated cancer cells

Project description:Expression data from sulfisoxazole-treated cancer cells

| PRJNA483940 | ENA

Expression data from liver cancer cell line Hep3B

Project description:Expression data from liver cancer cell line Hep3B

| PRJNA428723 | ENA

iTRAQ based proteomic analysis to reveal the mechanism of tigecycline resistance in Acinetobacter baumannii

Project description:The antibiotic resistance of A. baumannii has been increasing in recent years. There are still many questions unclear concerning the mechanism of tigecycline resistance in A. baumannii. iTRAQ based proteomic analysis were used to reveal the mechanism of tigecycline resistance in Acinetobacter baumannii.

2023-07-20 | PXD034784 | Pride

Human liver cancer cells Hep3B: Valeric acid treated vs. Control

Project description:Human liver cancer cells Hep3B: Valeric acid treated vs. Control

| PRJNA589081 | ENA

High-throughout sequencing of liver cancer cells treated Flavokawain C

Project description:High-throughout sequencing of liver cancer cells treated Flavokawain C

| PRJNA1011192 | ENA

Human liver cancer cells Hep3B: Valeric acid treated vs. Control

Project description:Transcriptional profiling of human liver cancer cells (Hep3B) treated with valeric acid compared to control.

2021-11-12 | GSE140280 | GEO

Characterization of Chemotherapy-treated PyMT Liver Matrisome

Project description:Metastasis accounts for 90% of cancer-related deaths, yet the mechanisms by which cancer cells colonize secondary organs remain poorly understood. For breast cancer patients, metastasis to the liver is associated with poor prognosis and a median survival of 6 months. Standard of care is chemotherapy, but recurrence occurs in 30% of patients. Systemic chemotherapy has been shown to induce hepatotoxicity and fibrosis, but how chemotherapy impacts the composition of the liver extracellular matrix (ECM) remains unknown. Individual ECM proteins drive tumor cell proliferation and invasion, features that are essential for metastatic outgrowth in the liver. Here, we characterize the liver ECM of tumor-bearing mice treated with and without chemotherapy using the MMTV-PyMT transgenic model of breast cancer. We identify distinct drug-specific changes induced by commonly used cytotoxic chemotherapies. We identify Collagen V as an ECM protein that is more abundant in livers isolated from paclitaxel-treated mice and identify mechanisms of Collagen V driven invasion via ECM organization and signaling through α1β1 integrins.

2022-10-05 | PXD036736 | Pride

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