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

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

PROVIDER: PRJNA658994 | ENA |

REPOSITORIES: ENA

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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

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

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-dependent transcriptomic changes in resistant basal cell carcinoma cell line

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

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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

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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

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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

Chromatin accessibility analysis of adipose progenitors (AP).

Project description:Chromatin accessibility analysis of adipose progenitors (AP).

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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)

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Genome-wide chromatin accessibility analysis of MRTF-active subpopulations in human 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. Here, we use three surface markers (LYPD3, TACSTD2, and LY6D) to isolate the nMRTF subpopulation and analyze chromatin accessibility profiles.

2020-08-25 | GSE156853 | GEO

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