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

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

PROVIDER: PRJNA836102 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19053070_1.fastq.gz	Fastqsanger.gz
	SRR19053070_2.fastq.gz	Fastqsanger.gz
	SRR19053071_1.fastq.gz	Fastqsanger.gz
	SRR19053071_2.fastq.gz	Fastqsanger.gz
	SRR19135368_1.fastq.gz	Fastqsanger.gz

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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 [ChIP-Seq]

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

| PRJNA834756 | 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 [cell line]

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

2022-05-10 | GSE202427 | GEO

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 [tumors]

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

2022-05-10 | GSE202426 | GEO

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

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

2022-05-06 | GSE202123 | GEO

Neo-Adjuvant Oncolytic Virotherapy Prior to Surgery Sensitizes Triple-Negative Breast Cancer to Immune Checkpoint Therapy

Project description:Triple-negative breast cancer (TNBC) is an aggressive disease for which treatment options are limited and associated with severe toxicities. In this experiment we evaluated the response of 2 murine TNBC models to oncolytic Maraba virus infection.

2018-10-01 | GSE104737 | GEO

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

Cholesterol biosynthesis inhibition synergizes with AKT inhibitors in triple-negative breast cancer

Project description:Triple-negative breast cancer (TNBC) is responsible for a disproportionate number of breast cancer deaths due to its molecular heterogeneity, high recurrence rate and lack of targeted therapies. Dysregulation of the phosphoinositide 3-kinase (PI3K)/AKT pathway occurs in approximately 50% of TNBC patients. We performed a genome-wide negative selection CRISPR/Cas9 screen with PI3K and AKT inhibitors to identify targetable synthetic lethalities in TNBC. We found that cholesterol homeostasis is a collateral vulnerability with AKT inhibition. Disruption of cholesterol homeostasis with pitavastatin synergized with AKT inhibition to induce TNBC cytotoxicity in vitro, in mouse TNBC xenografts and in patient-derived organoids of estrogen receptor (ER)-negative breast cancer. Neither ER-positive breast cancer cell lines nor ER-positive organoids were sensitive to combined AKT inhibitor and pitavastatin. Mechanistically, TNBCs show dysregulated SREBP-2 activation in response to single agent or combination AKT inhibitor and pitavastatin, and this was rescued by inhibition of the cholesterol trafficking protein Niemann-Pick C1 (NPC1). NPC1 loss promoted lysosomal cholesterol accumulation, decreased endoplasmic reticulum cholesterol levels and promoted SREBP-2 activation. Taken together, these data identify a TNBC-specific vulnerability to the combination of AKT inhibitors and pitavastatin mediated by dysregulated cholesterol trafficking. This work motivates combining AKT inhibitors with pitavastatin as a therapeutic modality in TNBC.

2024-01-14 | GSE252944 | GEO

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