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Effects of AEBP1 knockdown on gene expression profiles in cancer-associated fibroblasts

ABSTRACT: Effects of AEBP1 knockdown on gene expression profiles in cancer-associated fibroblasts

PROVIDER: PRJNA980558 | ENA |

REPOSITORIES: ENA

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Effects of AEBP1 knockdown on gene expression profiles in cancer-associated fibroblasts

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Project description:We recently identified adipocyte enhancer binding protein 1 (AEBP1) as a novel cancer stroma-associated gene and reported that AEBP1 activates cancer-associated fibroblasts in oral cancer. In this study, we show that AEBP1 is negatively associated with skeletal muscle cell differentiation. We found that AEBP1 is downregulated during the diffraction of human skeletal muscle myoblasts (HSMMs). Microarray analysis revealed that knockdown of AEBP1 significantly upregulated a number of genes associated with myogenesis in HSMMs. Notably, co-culture of HSMMs with oral squamous cell carcinoma cells resulted in downregulation of muscle-related genes and upregulation of AEBP1 in HSMMs.

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Project description:AEBP1 has been identified as a transcriptional repressor playing a significant role in adipogenesis. Recently, we have found that AEBP1 is specifically upregulated in primary glioblastoma. We have used gene silencing to identify genes perturbed upon AEBP1 downregulation and ChIP-chip technique to identify its genomic targets of binding and regulation to understand the un-annotated/undescribed role of this transcription factor in gliomagenesis. Cells either mock silenced or silenced using siRNA against AEBP1 were harvested at 46hrs post transfection. Gene expression was profiled for control and AEBP1 silenced cells. comparison of AEBP1/Rabbit IgG/ Glial cells

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Targeting of glioma stem-like cells with a parthenolide derivative ACT001 through inhibition of AEBP1/PI3K/AKT signaling

Project description:Glioblastoma (GBM) is the most lethal primary brain tumor in adults with a median survival of around 15 months. A potential treatment strategy involves targeting glioma stem-like cells (GSCs) that are able to initiate, maintain, and repopulate the tumor mass. Here, we identify ACT001, a parthenolide derivative, targeting GSCs through regulation of adipocyte enhancer binding protein 1 (AEBP1) signaling.GSCs exhibit high response to ACT001 in compared with normal human astrocytes. AEBP1 is a putative target of ACT001 by RNA-Seq analysis, which expression associates with prognosis of GBM patients. Knockdown of AEBP1 inhibits GSC proliferation whereas ectopic expression of AEBP1 increases GSC proliferation and xenograft tumor growth. AEBP1 overexpression also attenuates ATC001-inhibited GSC orthotopic xenograft tumor growth. Treatment with ACT001 or PI3K inhibitor or AEBP1 depletion decreases AKT phosphorylation and GSC proliferation. However, constitutive AKT activation rescues ACT001 treatment or AEBP1 knockdown-inhibited cell proliferation. Additionally, ACT001 blocks TGF-β-activated AEBP1/AKT signaling in GSCs. ACT001 exhibits antitumor activity either as a single agent or in combination with SHP099, which provides significant survival benefits for GSC xenograft tumor -bearing animals.

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