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CREB5 promotes tumorigenicity and upregulates druggable cell surface modalities in basal-like breast cancer

ABSTRACT: CREB5 promotes tumorigenicity and upregulates druggable cell surface modalities in basal-like breast cancer

PROVIDER: PRJNA1193078 | ENA |

REPOSITORIES: ENA

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CREB5 promotes tumorigenicity and upregulates druggable cell surface modalities in basal-like breast cancer

Project description:Basal-like breast cancers (BLBC), of which many are triple negative, have poor outcomes due to the limited targeted therapies available for patients. To address this need, we examined the clinical correlates and functional properties of CREB5, a transcription factor commonly amplified or overexpressed in other metastatic cancers. Using transcriptomic data from TCGA and METABRIC, we found BLBCs harbored the highest levels of CREB5 expression compared to other BC subtypes and that CREB5-high tumors had poor outcomes. In patient-matched primary and metastatic biopsies, CREB5 expression was robust and further increased in BLBCs that develop brain metastasis. CREB5 overexpression in 2 BLBC cell lines increased cell viability, formation of tumorspheres, and led to substantial increases in mRNA and cell surface expression of IL13RA2, a stem cell-like gene in brain cancers. IL13RA2 is a current CAR-T cell target in gliomas, and our work nominates IL13RA2 as a novel potential target in BLBCs.

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Creb5 controls its own expression and directly induces the joint-interzone regulatory program [RNAseq_Sox9_GFP]

Project description:Our prior work indicated that the transcription factor Creb5 plays a crucial role in the genesis of synovial joints. Here, we perform an integrative analysis of the transcriptome, chromatin accessibility, and Creb5-chromatin occupancy in Creb5-expressing synovial joint progenitor cells. This analysis revealed that Creb5 directly binds to both its own two promoters and to the regulatory regions of the early joint markers, Gdf5 and Sfrp2; each of whose expression in the joint-interzone is Creb5-dependent. Functional enhancer analysis indicated that Creb5 binding sites in its own two promoters are necessary for these sequences to drive transgene expression in a pattern that mimics endogenous Creb5 expression. While Creb5 directly regulates both Gdf5 and Sfrp2 expression in the inner joint-interzone by binding to either CREs or TREs in their regulatory elements, Creb5 activates Barx1 expression specifically in the outer joint-interzone; and thus initiates both the formation of the joint-interzone and regionalization of cell fates within this tissue.

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Creb5 controls its own expression and directly induces the joint-interzone regulatory program [RNAseq_Prx1]

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Creb5 controls its own expression and directly induces the joint-interzone regulatory program [ATACseq_Sox9_GFP]

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Effects of CREB5 overexpression on gene expression in Hepatocellular Carcinoma HepG2 cells

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