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Triple therapy reduced metastasis in triple-negative breast cancer

ABSTRACT: Purpose: To understand the underlying mechanisms of oncolytic virus therapy in breast cancer. Methods: The primary tumors of 4T1 in BALB/C mice were extracted and analyzed by RNA-seq. Results: In consistent with previous studies, we found some anti-tumor factors were up-regulated. Interestingly, several immunosupressive genes were activited. Conclusion: Our study identified the intercellular and intercellular factors restricting the optimized oHSV efficacy and supported the rationally designed triple therapy for clinical translation.

ORGANISM(S): Mus musculus

PROVIDER: GSE207977 | GEO | 2025/07/12

REPOSITORIES: GEO

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Triple therapy reduced metastasis in triple-negative breast cancer.

Project description:Purpose: To understand the underlying mechanisms of oncolytic virus therapy in breast cancer. Methods: The primary tumors of 4T1 in BALB/C mice were exstracted and analyzed by RNA-seq. Results: In consistent with previous studies, we found some anti-tumor factors were up-regulated. Interestingly, several immunosupressive genes were activited. Conclusion: Our study identified the intercellular and intracellular factors restricting the optimized oHSV efficacy and supported the rationally designed triple therapy for clinical translation.

2023-05-01 | GSE201760 | GEO

Transcription profiling of human MPNST cancer cells infected with G207 an oncolytic HSV

Project description:We used microarrays to identify genes regulated during oncolytic HSV infection. Oncolytic herpes simplex viruses (oHSV) are promising anticancer therapeutics. We sought to identify alterations in gene expression during oHSV infection of human cancer cells. Human malignant peripheral nerve sheath tumor (MPNST) cells were infected with G207, an ICP34.5-deleted oHSV previously evaluated in clinical trials. G207-infected cells demonstrated massive degradation of cellular mRNAs, while a subset were upregulated. A gene signature of 21 oHSV-induced genes contained 7 genes known to be HSV-induced. Go ontology classification revealed that a majority of upregulated genes are involved in Jak/STAT signaling, transcriptional regulation, nucleic acid metabolism, protein synthesis and apoptosis. Ingenuity-defined functional networks highlighted nodes for AP-1 subunits and interferon signaling via STAT1, SOCS1, SOCS3 and RANTES. Upregulation of SOCS1 correlated with sensitivity of MPNST lines to G207 and depletion of SOCS1 reduced virus replication >1-log. The transcriptome of oHSV-induced genes may predict oncolytic efficacy and provides rationale for next generation oncolytics. Experiment Overall Design: 5 human MPNST cancer cell lines were infected with G207 or mock infected for 6 hours followed by RNA extraction and hybridization on Affymetrix microarrays.

2008-06-16 | E-GEOD-8717 | biostudies-arrayexpress

FEC + OV treatment of TNBC tumors

Project description:E0771 subcutaneous tumors in C57/Bl6 mice were treated with saline, FEC (chemotherapy), oHSV-1 (oncolytic virus) or FEC + oHSV-1

2021-06-21 | GSE152698 | GEO

Tetracycline-Inducible Cyr61 effect on LN229 glioma cells

Project description:Glioblastoma multiforme is the most common and aggressive form of brain cancer. The use of oncolytic HSV-1 (oHSV) to selectively target brain cancer cells leading to their lytic destruction has shown to be very promising in a preclinical setting, but is lacking efficacy in clinical trials. Cyr61, a secreted extracellular matrix protein which functions to promote angiogenesis, migration, proliferation and tumorigenesis, was found to be upregulated rapidly following oHSV infection. Here we show, using microarray analysis, that Cyr61 expression leads to the induction of several genes with type 1 interferon function. We show that Cyr61 mediated type 1 IFN induction is through its interaction with integrin alpha6beta1 on the cell surface and results in oHSV inhibition, reducing the efficacy of this therapy. We used microarray to detail the global program of gene expression underlying Cyr61 mediated oncolytic HSV-1 inhibition and identified distinct classes of up-regulated genes during this process. Tetracycline-Inducible glioma cells expressing Cyr61 protein in the presence of doxycycline were treated with or without doxycycline for 24 hours. RNA was extracted and hybridized on Affymetrix microarray. Two groups: Â± dox to induce cyr61, performed in triplicate.

2012-04-03 | E-GEOD-29384 | biostudies-arrayexpress

IDH status dictates oHSV mediated metabolic reprogramming affecting anti-tumor immunity

Project description:Identification of IDH mutations has uncovered the crucial role played by metabolism in glioma-genesis. Oncolytic herpes virus (oHSV) therapy initiates direct tumor debulking by tumor lysis and also activates antitumor immunity however little is known about the role of glioma metabolism in determining oHSV efficacy. Here we identified that oHSV therapy rewired central carbon metabolism with increased glucose utilization towards oxidative phosphorylation and shuttled glutamine towards reductive carboxylation in IDH wildtype (wt) glioma. The switch in metabolism resulted in increased lipid synthesis, and cellular ROS. PKC induced ACSL4 in oHSV treated cells led to lipid peroxidation and ferroptosis. Ferroptosis was critical to launch an antitumor immune response important for efficacy. Mutant IDH (IDHR132H) gliomas are incapable of reductive carboxylation and hence ferroptosis. Pharmacological blockade of IDHR132H induced ferroptosis and antitumor immunity. This study provides a rationale to treat high grade IDHR132H glioma patients under oHSV treatment with IDHR132H inhibitor.

2025-04-02 | GSE289317 | GEO

m1A inhibition fuels oncolytic virus-elicited antitumor immunity via downregulating PD-L1 expression

Project description:RNA N1-methyladenosine methylation (m1A) modification is critical in regulating mRNA translation and thus protein synthesis, but the role of m1A modification in the occurrence, progression, and immunotherapy of head and neck squamous cell cancer (HNSCC) remains largely unknown. In Tgfbr1/Pten 2cKO mice, we found that the spontaneous neoplastic transformation of oral mucosa is accompanied by elevated levels of m1A modification. Analysis of m1A-associated genes identified TRMT61A as the key m1A writer associated with cancer progression, and poor prognosis. Mechanically, TRMT61A-induced tRNA-m1A modification promotes MYC protein synthesis and subsequent programmed death-ligand 1 (PD-L1) expression. In Tgfbr1/Pten 2cKO mice, RNA-m1A modification levels are also elevated in tumors that developed resistance to oncolytic herpes simplex virus (oHSV) treatment. Therapeutic inhibition of m1A modification sustains oncolytic virus-induced antitumor immunity and reduces tumor growth, providing a promising strategy for alleviating resistance to oHSV therapy. These findings indicate that m1A inhibition can prevent immune escape after oHSV therapy by reducing the expression of PD-L1. Our results provide a mutually reinforcing strategy for clinical combination immunotherapy.

2024-03-31 | GSE247024 | GEO

Expression data from Human MPNST cancer cells infected with G207 and oncolytic HSV

2007-08-08 | GSE8717 | GEO

Tetracycline-Inducible Cyr61 effect on LN229 glioma cells

2012-04-04 | GSE29384 | GEO

Single cell RNA-sequencing of M002 oHSV-treated murine glioblastoma

Project description:In this study, we evaluated the effects of M002 oncolytic herpes simplex virus (oHSV) in a syngeneic intracranial glioblastoma stem cell model. We harvested tumor-bearing mouse brain tissue 45 days post-injection of M002 oHSV and performed single-cell RNA-sequencing (scRNA-seq).

2024-12-03 | GSE246895 | GEO

oHSV Drives Tertiary Lymphoid Structure Boosting Oral Cancer Immunotherapy

Project description:The formation of TLSs induced by oncolytic virus treatment can enhance the anti-tumor response of oral cancer. Therefore, oncolytic virotherapy in vivo is a good strategy. To understand the mechanism of post-treatment changes, we collected oHSV-treated tumors for RNA-seq.

2025-01-08 | GSE262913 | GEO

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