Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chromatin accessibility analysis uncovers TFAP2A as a regulator on pro-angiogenesis of acquired resistance to anlotinib

ABSTRACT: Chromatin accessibility analysis uncovers TFAP2A as a regulator on pro-angiogenesis of acquired resistance to anlotinib

PROVIDER: PRJNA595696 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10693400_1.fastq.gz	Fastqsanger.gz
	SRR10693400_2.fastq.gz	Fastqsanger.gz
	SRR10693401_1.fastq.gz	Fastqsanger.gz
	SRR10693401_2.fastq.gz	Fastqsanger.gz
	SRR10693402_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Chromatin accessibility analysis uncovers TFAP2A as a regulator on pro-angiogenesis of acquired resistance to anlotinib

Project description:Anlotinib, a multitarget agent a multi-target agent that inhibits tumor proliferation and angiogenesis, has been demonstrated to be effective for non-small cell lung cancer (NSCLC) at third-line or over third-line. However, the underlying mechanisms of anlotinib acquired-resistance is still unclear. Here we performed chromatin accessibility profiling on anlotinib-resistant NCI-H1975 and wild-type NCI-H1975. By integrating with transcriptome analysis, we found that anlotinib resistance was due to increased angiogenic capacity, and revealed that TFAP2A was involved in anlotinib resistance. Next, TFAP2A was knock-down in anlotinib-resistant cells and RNAseq was performed to see down-regulated genes with TFAP2A KD.

2020-11-09 | GSE142031 | GEO

Role of Anlotinib-induced CCL2 decrease in anti-angiogensis and response prediction for Non-Small Cell Lung Cancer therapy

Project description:Purpose: Our previous clinical trials have been demonstrated that Anlotinib can inhibit tumor growth upon refractory advanced non-small cell lung cancer (NSCLC) patients with the possibility mechanism of anti-angiogenesis. The present study sought to reveal the underlying molecular mechanism of Anlotinib-induced anti-angiogenesis in advanced NSCLC. Experimental Design: Computed tomography (CT) was used to evaluate the treatment effect of Anlotinib upon refractory advanced NSCLC patients. Transcriptome profiling was performed to identify the key gene expression alteration in NCI-H1975 cells before and after Anlotinib treatment. NCI-H1975 derived xenograft model was applied to investigate treatment effect and verify anti-angiogenesis mechanism of Anlotinib. Results: Anlotinib induces tumor cytotoxicity on refractory advanced NSCLC patients, NCI-H1975 derived xenograft models and lung adenocarcinoma cell lines. Transcriptome profiling revealed CCL2 blockade could be responsible for Anlotinib-induced anti-angiogenesis. NCI-H1975 derived xenograft model demonstrated Anlotinib-induced CCL2 blockade play an important role in anti-angiogenesis. Conclusions: This study not only offered the first evidence that Anlotinib inhibits angiogenesis via blocking CCL2 expression, but also provided a novel theoretical basis for the application of Anlotinib in advanced NSCLC patients.

2018-11-30 | E-MTAB-5997 | biostudies-arrayexpress

Transcriptome profiling of Anlotinib-resistant NCI-H1975 and Anlotinib-treated Anlotinib-resistant NCI-H1975

Project description:Further to our previous study (E-MTAB-5997), here we performed transcriptome profiling on Anlotinib-resistant NCI-H1975 and Anlotinib-treated Anlotinib-resistant NCI-H1975, and would like to understand the effects of Anlotinib on Anlotinib-resistant NCI-H1975 cell, compare the different transcriptome profiling on NCI-H1975 cells and Anlotinib-resistant NCI-H1975 cells, sought to find the biomarker for explaining Anlotinib resistance.

2019-07-01 | E-MTAB-7068 | biostudies-arrayexpress

Pancreatic cancer cells treated with anlotinib

Project description:Aberrant regulation of angiogenesis involves in the growth and metastasis of tumors, but angiogenesis inhibitors fail to improve overall survival of pancreatic cancer patients in previous phase III clinical trials. A comprehensive knowledge of the mechanism of angiogenesis inhibitors against pancreatic cancer is helpful for clinical purpose and for the selection of patients who might benefit from the inhibitors. In this work, multi-omics analyses (transcriptomics, proteomics and phosphoproteomics profiling) were carried to delineate the mechanism of anlotinib, a novel angiogenesis inhibitor, against pancreatic cancer cells.

2021-09-09 | PXD023344 | Pride

Chromatin accessibility analysis reveals that TFAP2A promotes angiogenesis in acquired resistance to anlotinib in lung cancer cells.

Project description:Anlotinib, a multitarget tyrosine kinase inhibitor, is effective as a third-line treatment against non-small cell lung cancer (NSCLC). However, acquired resistance occurs during its administration. To understand the molecular mechanisms of anlotinib resistance, we characterized chromatin accessibility in both the parental and anlotinib-resistant lung cancer cell line NCI-H1975 through ATAC-seq. Compared with the parental cells, we identified 2666 genomic regions with greater accessibility in anlotinib-resistant cells, in which angiogenesis-related processes and the motifs of 21 transcription factors were enriched. Among these transcription factors, TFAP2A was upregulated. TFAP2A knockdown robustly diminished tumor-induced angiogenesis and partially rescued the anti-angiogenic activity of anlotinib. Furthermore, transcriptome analysis indicated that 2280 genes were downregulated in anlotinib-resistant cells with TFAP2A knocked down, among which the PDGFR, TGF-β, and VEGFR signaling pathways were enriched. Meanwhile, we demonstrated that TFAP2A binds to accessible sites within BMP4 and HSPG2. Collectively, this study suggests that TFAP2A accelerates anlotinib resistance by promoting tumor-induced angiogenesis.

| S-EPMC7608858 | biostudies-literature

Phosphoproteomics Data of pancreatic cancers cells treated with anlotinib

2021-09-09 | PXD023345 | Pride

Transcriptome profiling of Anlotinib-resistant NCI-H1975 and Anlotinib-treated Anlotinib-resistant NCI-H1975

Project description:Transcriptome profiling of Anlotinib-resistant NCI-H1975 and Anlotinib-treated Anlotinib-resistant NCI-H1975

| PRJEB27916 | ENA

RNA-seq of neuroblastoma syngeneic mouse models treated with anlotinib

Project description:We utilized murine neuroblastoma (NB) cell lines 975A2 and 9464D. Both cell lines were derived from spontaneous NB in the adrenal glands of TH-MYCN transgenic mice on a C57BL/6 background. 975A2 (2 x 106) and 9464D (1 x 106) tumor cells were subcutaneously implanted into the right back of 6-week-old C57BL/6 mice. When the mean tumor volume reached 30-50 mm3, the mice were randomized into individual treatment groups. After 9 days of anlotinib (6mg/kg) treatment, 3 mice from the treatment group and the vehicle group were sacrificed, and the tumors were snap-frozen with liquid nitrogen immediately after resection. Sequencing was performed at Beijing Novogene Co., Ltd., and the differentially expressed genes (DEGs) were subjected to enrichment analysis. The results showed that anlotinib treatment significantly upregulated immune-related pathways such as adaptive immune response, T cell activation, regulation of INF-γ production, lymphocyte chemotaxis, migration and adhesion, and cytokine receptor activity and significantly downregulated angiogenesis-related pathways such as cellular response to vascular endothelial growth factor stimulus and blood vessel endothelial cell proliferation involved in sprouting angiogenesis.

2021-11-25 | GSE179550 | GEO

Gene expression after human SW982 cells treated with anlotinib by a microarray profiling (Affymetrix)

Project description:Anlotinib could significantly suppresses synovial sarcoma proliferation in PDTX model and cell lines. To identify potential anlotinib targets in synovial sarcoma, we performed a microarray profiling (Affymetrix) in human SW982 cells treated with anlotinib.

2019-01-01 | GSE109468 | GEO

Gene expression after human PANC-1 cells treated with anlotinib by a microarray profiling (Affymetrix)

Project description:Anlotinib exerted cytotoxity on pancreatic cancer cells. To identify potential anlotinib targets in pancreatic cancer, we performed a microarray profiling (Affymetrix) in human PANC-1 cells treated with anlotinib.

2020-12-21 | GSE163574 | 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