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Genome-wide transcriptomic analysis of MRTF-active subpopulations in naïve human basal cell carcinoma

ABSTRACT: 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 transcriptomic profiles.

ORGANISM(S): Homo sapiens

PROVIDER: GSE156790 | GEO | 2020/08/25

REPOSITORIES: GEO

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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.

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

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

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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.

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Project description:Myocardin-related transcription factors (MRTFs) are robust co-activator of Serum Reponse Factor, and regulate cell adhesion and motility by controlling the transcription level of cytoskeletal components. In tumor progression, MRTFs has been reported to contribute to metastatic potential. Previously, we reported thymosin-ß4 (Tß4, which is encoded by Tmsb4x gene) as an activator of MRTFs. Enhanced expression of Tß4 is frequently observed during tumor progression, and associated with poor prognosis. However, the relationships between MRTFs and Tß4 in tumor progression are largely unknown. Here we analyze the effect of Tß4 knockout on the transcription levels of MRTFs-target genes. In particular, we focused on their functions in TGF-ß signaling because both MRTFs and Tß4 are down-stream effectors of TGF-ß.

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MRTF-SRF signaling is required for seeding of HSC/Ps in bone marrow during development

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