Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

KIAA1522 mediates resistance to cisplatin in lung adenocarcinoma cells

ABSTRACT: KIAA1522 mediates resistance to cisplatin in lung adenocarcinoma cells

PROVIDER: PRJNA609146 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11195445_1.fastq.gz	Fastqsanger.gz
	SRR11195445_2.fastq.gz	Fastqsanger.gz
	SRR11195446_1.fastq.gz	Fastqsanger.gz
	SRR11195446_2.fastq.gz	Fastqsanger.gz
	SRR11195447_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

KIAA1522 mediates resistance to cisplatin in lung adenocarcinoma cells

Project description:KIAA1522 is aberrantly over-expressed and predicts the outcome of platinum-base chemotherapy. Down-regulation of KIAA1522 sensitizes lung adenocarcinoma cells to cisplatin. To evaluate the molecular mechanisms underlying KIAA1522-induced cisplatin resistance. The RNA sequencing assays were performed in KIAA1522-depleted 889 cells.

2020-08-31 | GSE146072 | GEO

STAT3 contributes to cisplatin resistance, modulating EMT markers and the mTOR signaling in lung adenocarcinoma cells .

Project description:Lung cancer is the second leading cause of cancer death worldwide and is strongly associated with cisplatin resistance. The transcription factor STAT3 is constitutively activated in cancer cells and coordinates critical cellular processes as survival, self-renewal, and inflammation. In several types of cancer, STAT3 controls the development, immunogenicity, and malignant behavior of tumor cells while dictates the responsiveness to radio- and chemotherapy. It is known that STAT3 phosphorylation on Ser727 by mTOR is necessary for its maximal activation, but the crosstalk between STAT3 and mTOR signaling in cisplatin resistance remains elusive. In this study, using a proteomic label-based approach, we reveal important targets and signaling pathways increased and decreased in cisplatin-resistant A549 lung adenocarcinoma cells.

2022-02-17 | PXD025778 | Pride

Ito2019 - gefitnib resistance of lung adenocarcinoma caused by MET amplification

Project description:The model is based on publication: Mathematical analysis of gefitinib resistance of lung adenocarcinoma caused by MET amplification Abstract: Gefitinib, one of the tyrosine kinase inhibitors of epidermal growth factor receptor (EGFR), is effective for treating lung adenocarcinoma harboring EGFR mutation; but later, most cases acquire a resistance to gefitinib. One of the mechanisms conferring gefitinib resistance to lung adenocarcinoma is the amplification of the MET gene, which is observed in 5–22% of gefitinib-resistant tumors. A previous study suggested that MET amplification could cause gefitinib resistance by driving ErbB3-dependent activation of the PI3K pathway. In this study, we built a mathematical model of gefitinib resistance caused by MET amplification using lung adenocarcinoma HCC827-GR (gefitinib resistant) cells. The molecular reactions involved in gefitinib resistance consisted of dimerization and phosphorylation of three molecules, EGFR, ErbB3, and MET were described by a series of ordinary differential equations. To perform a computer simulation, we quantified each molecule on the cell surface using flow cytometry and estimated unknown parameters by dimensional analysis. Our simulation showed that the number of active ErbB3 molecules is around a hundred-fold smaller than that of active MET molecules. Limited contribution of ErbB3 in gefitinib resistance by MET amplification is also demonstrated using HCC827-GR cells in culture experiments. Our mathematical model provides a quantitative understanding of the molecular reactions underlying drug resistance.

2024-09-02 | BIOMD0000000827 | BioModels

DCBLD2 Mediates Epithelial-Mesenchymal Transition-Induced Metastasis by Cisplatin in Lung Adenocarcinoma

Project description:Growing evidence suggests that cisplatin and other chemotherapeutic agents promote tumor me-tastasis while inhibiting tumor growth, which is a critical issue in clinical practices. However, the role of chemotherapeutics in promoting tumor metastasis and the molecular mechanism involved are unclear. Here, we investigated the roles of cisplatin in promoting tumor metastasis in lung adenocarcinoma (LUAD). We demonstrated that cisplatin promoted epithelial-mesenchymal transition (EMT), cell motility, and metastasis in vitro and in vivo. The bioinformatic analysis and molecular biology approaches also indicated that DCBLD2 is a key gene that mediates cispla-tin-induced metastasis. DCBLD2 stabilizes β-catenin by phosphorylating GSK3β and transporting accumulated β-catenin to the nucleus to promote the expression of EMT-related transcriptional factors (TFs), ultimately resulting in tumor metastasis. We also identified that cisplatin aggravated DCBLD2 expression by phosphorylating ERK and hence the AP-1-driven transcription of DCBLD2. Furthermore, DCBLD2-specific siRNAs encapsulated by nanocarriers prominently in-hibits cisplatin-induced metastasis in vivo. Therefore, DCBLD2 plays a key role in cispla-tin-induced metastasis in LUAD and is a potential target for preventing chemotherapy-induced metastasis in vivo.

2021-03-09 | GSE168498 | GEO

DCBLD2 Mediates Epithelial-Mesenchymal Transition-Induced Metastasis by Cisplatin in Lung Adenocarcinoma

Project description:DCBLD2 Mediates Epithelial-Mesenchymal Transition-Induced Metastasis by Cisplatin in Lung Adenocarcinoma

| PRJNA707567 | ENA

Pulsed cisplatin treatment of A549 lung adenocarcinoma cells

Project description:A549 lung adenocarcinoma cells were pulsed for 2h with cisplatin and allowed to recover for 3 days. Cells were then FACS sorted based on size and enriched populations analysed for RNAseq.

2021-05-18 | GSE161800 | GEO

Pulsed cisplatin treatment of A549 lung adenocarcinoma cells

Project description:Pulsed cisplatin treatment of A549 lung adenocarcinoma cells

| PRJNA679554 | ENA

Noncoding RNA expression profiling of cisplatin-resistant cells derived from the A549 lung cell line (miRNA)

Project description:To determine the signaling networks that are dysregulated in cisplatin-resistant non-small cell lung cancer, noncoding RNA expression data were obtained from, and compared between, the lung adenocarcinoma cell line, A549, and its cisplatin-resistant derivative, A549/CDDP. Noncoding RNA expression data from a cisplatin-sensitive lung adenocarcinoma cancer cell line (A549) were collected and compared to noncoding RNA expression data from a cisplatin-resistant cell line (A549/CDDP). 3 independent experiments were completed for both the sensitive and resistant cell lines.

2013-01-15 | E-GEOD-43249 | biostudies-arrayexpress

Noncoding RNA expression profiling of cisplatin-resistant cells derived from the A549 lung cell line (lncRNA and mRNA)

2013-01-15 | E-GEOD-43493 | biostudies-arrayexpress

c-Fos mediates cell proliferation, invasion and drug-resistance of lung adenocarcinoma through MAPK signal pathway

Project description:Lung cancer is the main cause of cancer-related death in men and women all over the world. Lung adenocarcinoma (LUAD) is the most common histological subtype of lung cancer, with the overall 5-year survival rate is less than 20% . We found the mRNA expression of c-Fos in LUAD clinical samples was decreased significantly compared to adjacent normal control. Overexpression of c-Fos inhibited LUAD cell proliferation, colony formation, and induced cell apoptosis while c-Fos knockdown promoted cell proliferation, colony formation, and suppressed cell apoptosis. Cell cycle showed little difference after c-Fos knockdown but overexpression of c-Fos increased the distribution of G1 phase when decreased G2 phase cells. Knockdown of c-Fos reduced the sensitivity of LUAD cells to cisplatin but overexpression of c-Fos increased the efficacy of cisplatin both in vitro and in vivo. MAPK signaling pathway was enriched after c-Fos was overexpressed in LUAD cells. The expression of c-Jun, c-Myc and DUSP1 was greatly inhibited after c-Fos overexpression but incresed after c-Fos knockdown, which suggests c-Fos regulated MAPK signaling pathway in LUAD. Furthermore, c-Fos was shown to interact with c-Jun and overexpression of c-Jun partially recovered the expression of c-Jun, c-Myc and DUSP1 caused by c-Fos overexpression. Cell proliferation was also rescued when apoptosis was decreased followed by c-Jun overexpression. In contrast, knockdown of c-Jun inhibited cell proliferation and promoted cell apoptosis in LUAD cells when reduced the level of c-Jun, c-Myc and DUSP1. In summary, c-Fos inhibits cell proliferation, promotes apoptosis and increses cisplatin-sensitivity of lung adenocarcinoma cells via regulating MAPK signaling by interacting with c-Jun in certain LUADs.

2023-09-20 | GSE213590 | GEO

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