Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chromatin accessibility changes in experimentally-induced basal to squamous cell carcinoma transition (BST) upon EGFR/MAPK inhibitor treatments [ASZ_ATACseq_inhibitor]

ABSTRACT: Chromatin accessibility changes in experimentally-induced basal to squamous cell carcinoma transition (BST) upon EGFR/MAPK inhibitor treatments [ASZ_ATACseq_inhibitor]

PROVIDER: PRJNA741494 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14916023_1.fastq.gz	Fastqsanger.gz
	SRR14916023_2.fastq.gz	Fastqsanger.gz
	SRR14916024_1.fastq.gz	Fastqsanger.gz
	SRR14916024_2.fastq.gz	Fastqsanger.gz
	SRR14916025_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Chromatin accessibility changes in experimentally-induced basal to squamous cell carcinoma transition (BST) upon EGFR/MAPK inhibitor treatments [ASZ_ATACseq_inhibitor]

Project description:Basal cell carcinoma may undergo BST spontaneously or upon Hedgehog targeting therapy. We identified that modulation of Ras/MAPK or TGFb signaling drive BST. Here, we induce Ras/MAPK and/or abrogate TGFb signaling to induce BST. Alternatively we drive c-FOS to induce BST. Here, we analyze chromatin accessibility profiles upon c-FOS activation

2021-10-20 | GSE178914 | GEO

Chromatin accessibility changes in experimentally-induced basal to squamous cell carcinoma transition (BST)

Project description:Basal cell carcinoma may undergo BST spontaneously or upon Hedgehog targeting therapy. We identified that modulation of Ras/MAPK or TGFb signaling drive BST. Here, we induce Ras/MAPK and/or abrogate TGFb signaling to induce BST. Alternatively we drive c-FOS to induce BST. In these various experimentally-induced model of BST, we analyze chromatin accessibility profiles upon Ras/MAPK activation and/or TGFb signaling abrogation. We also analyze chromatin accessibility profiles upon c-FOS activation.

2021-10-05 | GSE161009 | GEO

Transcriptional changes in experimentally-induced basal to squamous cell carcinoma transition (BST) upon treatment with small molecule inhibitors [ASZ_RNAseq_inhibitor]

Project description:Basal cell carcinoma may undergo BST spontaneously or upon Hedgehog targeting therapy. We identified that either modulation of Ras/MAPK or TGFb signaling or c-FOS induction could drive BST. Enhanced EGFR signaling has been implicated during BST. Here, we analyze transcriptional profiles upon c-FOS induction when cells are treated with EGFR signaling inhibitors afatinib (5uM) and UO126 (10uM).

2021-10-20 | GSE166596 | GEO

Transcriptional changes in experimentally-induced basal to squamous cell carcinoma transition (BST) [ASZ_RasV12_TGFbR1_RNAseq]

Project description:Basal cell carcinoma may undergo BST spontaneously or upon Hedgehog targeting therapy. We identified that modulation of Ras/MAPK or TGFb signaling drive BST. Here, we induce Ras/MAPK and/or abrogate TGFb signaling to induce BST. Alternatively we drive c-FOS to induce BST. Here, we analyze transcriptional profiles upon Ras/MAPK activation and/or TGFb signaling abrogation.

2021-10-20 | GSE166593 | GEO

Transcriptional changes in experimentally-induced basal to squamous cell carcinoma transition (BST) [ASZ_cFOS_RNAseq]

2021-10-05 | GSE166595 | GEO

DNA binding profile of c-FOS in experimentally-induced basal to squamous cell carcinoma transition (BST)

2021-10-20 | GSE168374 | GEO

Neocarzilin inhibits cancer cell proliferation via BST-2 degradation resulting in lipid raft trapped EGFR

Project description:Neocarzilin (NCA) is a natural product exhibiting potent anti-migratory as well as anti-proliferative effects. While the vesicle amide transport protein 1 (VAT-1) was previously shown to inhibit migration upon NCA binding, the molecular mechanisms responsible for impaired proliferation remained elusive. We here introduce a chemical probe closely resembling the structural and stereochemical features of NCA and unravel bone marrow stromal antigen 2 (BST-2) as a second major target in cancer cells. The antiproliferative mechanism of NCA was confirmed in corresponding BST-2 knockout (KO) cells which were less sensitive to compound treatment. Vice versa, overexpression of the target in the KO reduced proliferation comparable to wild type (wt) cells. Whole proteome mass-spectrometric (MS) analysis of NCA treated wt and KO cancer cells unraveled affected pathways linked to EGFR signaling and demonstrated reduced levels of BST-2 upon NCA treatment. In-depth analysis of BST-2 levels in response to proteasome and lysosome inhibitors, confirmed a lysosomal degradation path upon NCA treatment. As BST-2 is mediating the release of EGFR from lipid rafts to turn on proliferation signaling pathways, reduced BST-2 levels led to attenuated phosphorylation of EGFR and downstream targets. Furthermore, fluorescence microscopy confirmed colocalization of BST-2 and lipid rafts in presence of NCA. Overall, NCA represents a versatile anti-cancer natural product with a unique dual mode of action and unconventional inhibition of proliferation via BST-2 degradation.

2024-11-26 | PXD050453 | Pride

Transcriptional changes in experimentally-induced basal to squamous cell carcinoma transition (BST) [ASZ_RasV12_TGFbR1_RNAseq]

Project description:Transcriptional changes in experimentally-induced basal to squamous cell carcinoma transition (BST) [ASZ_RasV12_TGFbR1_RNAseq]

| PRJNA701325 | ENA

Chromatin accessibility changes in experimentally-induced basal to squamous cell carcinoma transition (BST)

Project description:Chromatin accessibility changes in experimentally-induced basal to squamous cell carcinoma transition (BST)

| PRJNA675105 | ENA

Transcriptional changes in experimentally-induced basal to squamous cell carcinoma transition (BST) [ASZ_cFOS_RNAseq]

Project description:Transcriptional changes in experimentally-induced basal to squamous cell carcinoma transition (BST) [ASZ_cFOS_RNAseq]

| PRJNA701331 | ENA