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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE202428 | GEO | 2022/05/08

REPOSITORIES: GEO

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

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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.

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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

2022-05-10 | GSE202427 | 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

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

Oncolytic Urabe mumps virus: A promising virotherapy for triple-negative breast cancer.

Project description:Historically, the clinical utility of oncolytic virotherapy as a treatment for a wide range of cancer types was first demonstrated by three pilot human clinical trials conducted in Japan in the 1970s and 1980s using a wild-type Urabe mumps virus (MuV) clinical isolate. Using a sample of the actual original oncolytic Urabe MuV clinical trial virus stock (MuV-U-Japan) used in these Japanese clinical trials, we found that MuV-U-Japan consisted of a wide variety of very closely related Urabe MuVs that differed by an average of only three amino acids. Two MuV-U-Japan isolates, MuV-UA and MuV-UC, potently killed a panel of established human breast cancer cell lines in vitro, significantly extended survival of nude mice with human triple-negative breast cancer (TNBC) MDA-MB-231 tumor xenografts in vivo, and demonstrated significant killing activity against breast cancer patient-derived xenograft (PDX) cell lines grown as 3D organoids, including PDXs from patients resistant to anthracycline- and taxane-based chemotherapy. We also report success in developing a large-scale MuV-U production and purification process suitable for supporting Investigational New Drug applications for clinical trials. This study demonstrates the suitability of the MuV-UC virus for translation to modern clinical trials for treating patients with TNBC.

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Enhanced mitochondrial fission suppresses signaling and metastasis in triple-negative breast cancer.

Project description:BackgroundMitochondrial dynamics underlies malignant transformation, cancer progression, and response to treatment. Current research presents conflicting evidence for functions of mitochondrial fission and fusion in tumor progression. Here, we investigated how mitochondrial fission and fusion states regulate underlying processes of cancer progression and metastasis in triple-negative breast cancer (TNBC).MethodsWe enforced mitochondrial fission and fusion states through chemical or genetic approaches and measured migration and invasion of TNBC cells in 2D and 3D in vitro models. We also utilized kinase translocation reporters (KTRs) to identify single cell effects of mitochondrial state on signaling cascades, PI3K/Akt/mTOR and Ras/Raf/MEK/ERK, commonly activated in TNBC. Furthermore, we determined effects of fission and fusion states on metastasis, bone destruction, and signaling in mouse models of breast cancer.ResultsEnforcing mitochondrial fission through chemical or genetic approaches inhibited migration, invasion, and metastasis in TNBC. Breast cancer cells with predominantly fissioned mitochondria exhibited reduced activation of Akt and ERK both in vitro and in mouse models of breast cancer. Treatment with leflunomide, a potent activator of mitochondrial fusion proteins, overcame inhibitory effects of fission on migration, signaling, and metastasis. Mining existing datasets for breast cancer revealed that increased expression of genes associated with mitochondrial fission correlated with improved survival in human breast cancer.ConclusionsIn TNBC, mitochondrial fission inhibits cellular processes and signaling pathways associated with cancer progression and metastasis. These data suggest that therapies driving mitochondrial fission may benefit patients with breast cancer.

| S-EPMC7275541 | biostudies-literature

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