Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

AP-1 and TGFb-dependent transcriptomic changes in resistant basal cell carcinoma cell line

ABSTRACT: AP-1 and TGFb-dependent transcriptomic changes in resistant basal cell carcinoma cell line

PROVIDER: PRJNA659018 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

AP-1 and TGFb-dependent transcriptomic changes in resistant basal cell carcinoma cell line

Project description:Tumor heterogeneity and lack of knowledge about resistant cell states remain a significant barrier to effective targeted cancer therapies. Basal cell carcinomas (BCCs) uniformly depend on Hedgehog (Hh)/Gli signaling for cell growth. We previously identified a nuclear myocardin-related transcription factor (nMRTF) resistance pathway that amplifies Gli1 activity, but nMRTF cell state and key factors driving its accumulation remain unknown. We have determined that AP-1 and TGFb transcription factor activity is essential to maintain MRTF activation. Here, we treat a murine BCC cell line with small molecule AP-1 and ALK5 inhibitors and analyze transcriptomic profiles.

2020-08-25 | GSE156789 | GEO

AP-1 and TGFb cooperativity drives non-canonical Hedgehog signaling in resistant basal cell carcinoma

Project description:AP-1 and TGFb cooperativity drives non-canonical Hedgehog signaling in resistant basal cell carcinoma

| PRJNA659351 | ENA

AP-1 dependent changes in chromatin accessibility in resistant basal cell carcinoma cell line

Project description:Tumor heterogeneity and lack of knowledge about resistant cell states remain a significant barrier to effective targeted cancer therapies. Basal cell carcinomas (BCCs) uniformly depend on Hedgehog (Hh)/Gli signaling for cell growth. We previously identified a nuclear myocardin-related transcription factor (nMRTF) resistance pathway that amplifies Gli1 activity, but nMRTF cell state and key factors driving its accumulation remain unknown. We have determined that AP-1 transcription factor activity is essential to maintain MRTF activation. Here, we treat a murine BCC cell line with small molecule AP-1 inhibitor and analyze chromatin accessibility profiles.

2020-08-25 | GSE156764 | GEO

AP-1 dependent changes in chromatin accessibility in resistant basal cell carcinoma cell line

Project description:AP-1 dependent changes in chromatin accessibility in resistant basal cell carcinoma cell line

| PRJNA658994 | ENA

DNA binding profile of c-FOS 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 and examine the DNA binding profile of the AP-1 transcription factor c-FOS.

2021-10-20 | GSE168374 | GEO

Analysis of AP-1 regulation on Smad3 genome-wide DNA binding sites in resistant basal cell carcinoma

Project description:Tumor heterogeneity and lack of knowledge about resistant cell states remain a significant barrier to effective targeted cancer therapies. Basal cell carcinomas (BCCs) uniformly depend on Hedgehog (Hh)/Gli signaling for cell growth. We previously identified a nuclear myocardin-related transcription factor (nMRTF) resistance pathway that amplifies Gli1 activity, but nMRTF cell state and key factors driving its accumulation remain unknown. Epigenetic analysis of isolated nMRTF human tumor subpopulations demonstrates that cooperative AP-1 and TGFß signaling drive nMRTF activation. In this study, we find that AP-1 signaling drives changes in chromatin accessibility leading to differential Smad3 DNA binding and a transcriptional program of upstream activators of Rho, including RhoGEFs, that facilitate nMRTF activity.

2020-08-25 | GSE142469 | 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

Analysis of AP-1 regulation on Smad3 genome-wide DNA binding sites in resistant basal cell carcinoma

Project description:Analysis of AP-1 regulation on Smad3 genome-wide DNA binding sites in resistant basal cell carcinoma

| PRJNA597071 | ENA

AP-1 and TGFb cooperativity drives non-canonical Hedgehog signaling in resistant basal cell carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-08-25 | GSE156855 | GEO

Transcriptional changes in experimentally-induced basal to squamous cell carcinoma transition (BST) [ASZ_cFOS_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 c-FOS induction.

2021-10-05 | GSE166595 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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