Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A strategy to personalize the use of radiation in patients with brain metastasis based on S100A9-mediated resistance

ABSTRACT: A strategy to personalize the use of radiation in patients with brain metastasis based on S100A9-mediated resistance

PROVIDER: PRJNA726153 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14356936.fastq.gz	Fastqsanger.gz
	SRR14356937.fastq.gz	Fastqsanger.gz
	SRR14356938.fastq.gz	Fastqsanger.gz
	SRR14356939.fastq.gz	Fastqsanger.gz
	SRR14356940.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 17

Similar Datasets

A strategy to personalize the use of radiation in patients with brain metastasis based on S100A9-mediated resistance

Project description:We report a strategy to personalize the use of radiotherapy on brain metastasis from lung cancer and breast cancer compatible with liquid biopsy and the use of a radiosensitizer.

2022-02-14 | GSE173554 | GEO

S100A9 is a mediator of the ID1 functions in metastasis

Project description:Metastasis is a major factor responsible for mortality in breast cancer patients. Id1 plays important roles in cell differentiation and promotes tumor angiogenesis, cell invasion and metastasis. Although Id1 is established as a critical factor for lung metastasis in breast cancer, the pathways and molecular mechanisms of Id1 functions in metastasis remains to be defined. Here we show that Id1 interacts with TFAP2A to suppress S100A9 expression. The expression of Id1 and S100A9 is inversely correlated in both breast cancer cell lines and clinical samples. We also find that S100A9 expression rescues the migratory and invasive phenotypes in vitro and metastasis in vivo induced by Id1 expression. S100A9 also suppresses the expression of known metastasis promoting factor RhoC activated by Id1 expression. Our results suggest that S100A9 mediates the functions of Id1 in breast cancer metastasis.

2017-08-29 | GSE53847 | GEO

Radiation-induced amphiregulin drives tumor metastasis

Project description:The anti-tumor effect of radiotherapy (RT) beyond the treatment field - the abscopal effect - has garnered much interest. By contrast, the potentially harmful impact of radiation in promoting metastasis is less well studied. Here, we show that RT induces the expression of epidermal growth factor receptor (EGFR) ligand amphiregulin (AREG) in tumor cells, which reprograms EGFR+ myeloid cells toward an immunosuppressive phenotype and reduces phagocytosis. This stimulates distant metastasis growth in both patients and pre-clinical murine tumor models. The inhibition of these tumor-promoting factors induced by RT may represent a novel therapeutic strategy to improve patient outcomes.

2025-03-05 | GSE291151 | GEO

Radiation-induced amphiregulin drives tumor metastasis

Project description:Radiation-induced amphiregulin drives tumor metastasis

| PRJNA1232101 | ENA

Resistance to Radiation Enhances Metastasis by Altering RNA Metabolism

Project description:The cellular programs that mediate therapy resistance are often important drivers of metastasis, a phenomenon that needs to be understood better to improve screening and treatment options for cancer patients. Although this issue has been studied extensively for chemotherapy, less is known about a causal link between resistance to radiation therapy and metastasis. We investigated this problem in triple-negative breast cancer (TNBC) and established that radiation resistant tumor cells have enhanced metastatic capacity, especially to bone. Resistance to radiation increases the expression of integrin b3 (ITGb3), which promotes enhanced migration and invasion. Bioinformatic analysis and subsequent experimentation revealed an enrichment of RNA metabolism pathways that stabilize ITGb3 transcripts. Specifically, the RNA binding protein heterogenous nuclear ribonucleoprotein L (HNRNPL), whose expression is regulated by Nrf2, mediates the formation of circular RNAs (circRNAs) that function as competing endogenous RNAs (ceRNAs) for the family of let-7 microRNAs that target ITGb3. Collectively, our findings identify a novel mechanism of radiation-induced metastasis that is driven by alterations in RNA metabolism.

2025-10-01 | GSE290005 | GEO

Biological effects of recombinant S100A8, recombinant S100A9, and recombinant S100A8/S100A9 on human renal tubular epithelial cells (HK-2)

Project description:In order to explore how S100A8 and S100A9 may participate in the kidney stone formation, we used recombinant S100A8, recombinant S100A9, or recombinant S100A8/S100A9 heterodimer to culture the HK-2 cells and then sequenced total cellular mRNAS.

2024-11-06 | GSE265848 | GEO

Resistance to Radiation Enhances Metastasis by Altering RNA Metabolism

Project description:Resistance to Radiation Enhances Metastasis by Altering RNA Metabolism

| PRJNA1225724 | ENA

Validation of a genomic classifier for prediction of metastasis following postoperative radiation therapy.

Project description:To test the hypothesis that a genomic classifier (GC) would predict biochemical failure (BF) and distant metastasis (DM) in men receiving radiation therapy (RT) after radical prostatectomy (RP).

2016-05-09 | GSE72291 | GEO

Expression data for murine colon carcinoma cell line CT26.WT stimulated with S100a8 or S100a9 recombinant protein

Project description:Damage-associated molecular pattern (DAMP) molecules S100A8 and S100A9 with well-known functions in inflammation, tumor growth and metastasis. It has been found to have promote tumor cell proliferation activity at low concentration . However, the mechanism underlying this remains unclear. In the current study, we performed genome expression profiling analysis using the Affymetrix genome wide microarray system to identify broad scale changes in gene expression associated with S100a8 or S100a9 recombinant protein stimulation in murine colon carcinoma cell line CT26.WT.

2015-11-29 | GSE53735 | GEO

The alarmin S100A9 hampers retroviral infection by limiting reverse transcription

Project description:We identified the alarmin S100A9 as a novel intracellular antiretroviral factor expressed in human monocyte-derived and skin-derived Langerhans cells (LC). The expression of S100A9 is significantly upregulated by the transforming growth factor beta in human monocyte-derived cells. We showed that S100A9 intracellular expression is decreased upon maturation and inversely correlated with an enhanced inversely correlates with the maturation level of LC and susceptibilityility to HIV-1 infection of LC. Furthermore, silencing of S100A9 in primary human LC relieves HIV-1 restriction while ectopic expression of S100A9 in various cell lines established an intrinsic resistance to both HIV-1 and MMLV infection by acting on reverse transcription. Mechanistically, the intracellular expression of S100A9 alters viral capsid uncoating and reverse transcription in a distal manner. Also, S100A9 demonstrates potent inhibitory effect against HIV-1 and MMLV reverse transcriptase (RTase) activity in-vitro in a divalent cation-dependent context. Our findings uncover an unexpected intracellular antiretroviral function of the human alarmin S100A9 and highlight a novel crosstalk betweenregulating antiretroviral immunity in Langerhans cells

2021-05-06 | GSE173939 | 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