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Manipulating Cholesterol Metabolism by oncolytic virus suppresses metastasis of triple-negative breast cancer [ChIP-Seq]

ABSTRACT: Investigate the role of FOXO3a in the ApoA1 induced KRT14 suppression.

ORGANISM(S): Mus musculus

PROVIDER: GSE202123 | GEO | 2022/05/06

REPOSITORIES: GEO

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Manipulating Cholesterol Metabolism by oncolytic virus suppresses metastasis of triple-negative breast cancer [tumors]

Project description:To investigate the effect of ADV or AAV encoding ApoA1 treatment on the gene expression of 4T1 tumor in vivo

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Manipulating Cholesterol Metabolism by oncolytic virus suppresses metastasis of triple-negative breast cancer [cell line]

Project description:To investigate the effect of ApoA1 mediated cholesterol efflux on the gene expression of 4T1 cells

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Manipulating Cholesterol Metabolism by oncolytic virus suppresses metastasis of triple-negative breast cancer

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

2022-05-08 | GSE202428 | GEO

Manipulating Cholesterol Metabolism by oncolytic virus suppresses metastasis of triple-negative breast cancer

Project description:Manipulating Cholesterol Metabolism by oncolytic virus suppresses metastasis of triple-negative breast cancer

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Manipulating Cholesterol Metabolism by oncolytic virus suppresses metastasis of triple-negative breast cancer [tumors]

Project description:Manipulating Cholesterol Metabolism by oncolytic virus suppresses metastasis of triple-negative breast cancer [tumors]

| PRJNA836105 | ENA

Manipulating Cholesterol Metabolism by oncolytic virus suppresses metastasis of triple-negative breast cancer [cell line]

Project description:Manipulating Cholesterol Metabolism by oncolytic virus suppresses metastasis of triple-negative breast cancer [cell line]

| PRJNA836104 | ENA

Manipulating Cholesterol Metabolism by oncolytic virus suppresses metastasis of triple-negative breast cancer [ChIP-Seq]

Project description:Manipulating Cholesterol Metabolism by oncolytic virus suppresses metastasis of triple-negative breast cancer [ChIP-Seq]

| PRJNA834756 | ENA

Apolipoprotein A1-Manipulated Cholesterol Efflux Subverts the Phagocytic Fragility of TAMs and Improves Oncolytic Viro-Immunotherapy in Glioblastoma [Tumor RNA-seq]

Project description:We found that overexpression of APOA1 in glioblastoma (GBM) promotes cholesterol efflux from TAMs and restores phagocytosis and antigen presentation. Therefore, we constructed a recombinant oncolytic adenovirus expressing APOA1 to carry the cholesterol regulatory elements of TAMs. AdV-APOA1 exhibited better antitumor effects than AdV-Ctrl in several orthotopic GBM tumor models. Further, we collected virus-treated GL261-CAR tumors for RNA-seq to reveal differences in biological processes between them. Specifically, intracranial 14-day GL261-CAR-bearing C57BL/6J mice were i.t. injected with 1 × 108 PFU AdV-Ctrl or 1 × 108 PFU AdV-APOA1. The tumor bulks were then collected to perform transcriptome RNA-seq analysis 3 days after virus injection.

2022-05-04 | GSE201976 | GEO

Oncolytic Herpes Simplex Virus Encoding IL12 Controls Triple-Negative Breast Cancer Growth and Metastasis.

Project description:Triple-negative breast cancer (TNBC) is a difficult-to-treat disease with high rates of local recurrence, distant metastasis, and poor overall survival with existing therapies. Thus, there is an unmet medical need to develop new treatment regimen(s) for TNBC patients. An oncolytic herpes simplex virus encoding a master anti-tumor cytokine, interleukin 12, (designated G47Δ-mIL12) selectively kills cancer cells while inducing anti-tumor immunity. G47Δ-mIL12 efficiently infected and killed murine (4T1 and EMT6) and human (HCC1806 and MDA-MB-468) mammary tumor cells in vitro. In vivo in the 4T1 syngeneic TNBC model, it significantly reduced primary tumor burden and metastasis, both at early and late stages of tumor development. The virus-induced local and abscopal effects were confirmed by significantly increased infiltration of CD45+ leukocytes and CD8+ T cells, and reduction of granulocytic and monocytic MDSCs in tumors, both treated and untreated contralateral, and in the spleen. Significant trafficking of dendritic cells (DCs) were only observed in spleens of virus-treatment group, indicating that DCs are primed and activated in the tumor-microenvironment following virotherapy, and trafficked to lymphoid organs for activation of immune cells, such as CD8+ T cells. DC priming/activation could be associated with virally enhanced expression of several antigen processing/presentation genes in the tumor microenvironment, as confirmed by NanoString gene expression analysis. Besides DC activation/priming, G47Δ-mIL12 treatment led to up-regulation of CD8+ T cell activation markers in the tumor microenvironment and inhibition of tumor angiogenesis. The anti-tumor effects of G47Δ-mIL12 treatment were CD8-dependent. These studies illustrate the ability of G47Δ-mIL12 to immunotherapeutically treat TNBC.

| S-EPMC7105799 | biostudies-literature

Apolipoprotein A1-Manipulated Cholesterol Efflux Subverts the Phagocytic Fragility of TAMs and Improves Oncolytic Viro-Immunotherapy in Glioblastoma [TAMs RNA-seq]

Project description:We found that TAMs in the glioblatoma (GBM) tumor microenvironment are enriched for cholesterol and highly express ABCA1/G1. To investigate the biological effects of enhancing cholesterol efflux of TAMs in GBM, we constructed APOA1-overexpressing GL261 cell line. We harvested tumor tissue and sorted these TAMs by anti-mouse F4/80 magnetic beads 17 days after intracranial transplantation of GL261-APOA1 cell line and control cells in immunocompetent C57 mice. Samples were subjected to transcriptome sequencing.

2022-05-04 | GSE201975 | GEO

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