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Single-cell RNA sequencing reveals a strong connection between Gadd45g upregulation and oncolytic HSV infection in tumor tissue

ABSTRACT: Single-cell RNA sequencing reveals a strong connection between Gadd45g upregulation and oncolytic HSV infection in tumor tissue

PROVIDER: PRJNA775970 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16611300.fastq.gz	Fastqsanger.gz
	SRR16611301.fastq.gz	Fastqsanger.gz
	SRR16611302.fastq.gz	Fastqsanger.gz
	SRR16611303.fastq.gz	Fastqsanger.gz
	SRR16611304.fastq.gz	Fastqsanger.gz

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Single-cell RNA sequencing reveals a strong connection between Gadd45g upregulation and oncolytic HSV infection in tumor tissue

Project description:The oncolytic effect of virotherapy derives from the intrinsic capability of the applied virus in selectively infecting and killing tumor cells. Although oncolytic viruses of various constructions have been shown to efficiently infect and kill tumor cells in vitro, the efficiency of these viruses to exert the same effect on tumor cells within tumor tissues in vivo has not been extensively investigated. Here we report our studies using single-cell RNA sequencing to comprehensively analyze the gene expression profile of tumor tissues following herpes simplex virus 2-based oncolytic virotherapy. Our data revealed the extent and cell types within the tumor microenvironment that could be infected by the virus. Moreover, we observed changes in the expression of cellular genes, including antiviral genes, in response to viral infection. One notable gene found to be upregulated significantly in oncolytic virus-infected tumor cells was Gadd45g, which is desirable for optimal virus replication. These results not only help reveal the precise infection status of the oncolytic virus in vivo, but also provide insight that may lead to the development of new strategies to further enhance the therapeutic efficacy of oncolytic virotherapy.

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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

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

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Single-cell RNA sequencing reveals a strong connection between <i>Gadd45g</i> upregulation and oncolytic HSV infection in tumor tissue.

Project description:The oncolytic effect of virotherapy derives from the intrinsic capability of the applied virus in selectively infecting and killing tumor cells. Although oncolytic viruses of various constructions have been shown to efficiently infect and kill tumor cells in vitro, the efficiency of these viruses to exert the same effect on tumor cells within tumor tissues in vivo has not been extensively investigated. Here we report our studies using single-cell RNA sequencing to comprehensively analyze the gene expression profile of tumor tissues following herpes simplex virus 2-based oncolytic virotherapy. Our data revealed the extent and cell types within the tumor microenvironment that could be infected by the virus. Moreover, we observed changes in the expression of cellular genes, including antiviral genes, in response to viral infection. One notable gene found to be upregulated significantly in oncolytic virus-infected tumor cells was Gadd45g, which is desirable for optimal virus replication. These results not only help reveal the precise infection status of the oncolytic virus in vivo but also provide insight that may lead to the development of new strategies to further enhance the therapeutic efficacy of oncolytic virotherapy.

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Project description:Oncolytic HSV-1 derived viruses are being developed for cancer treatment. Here we describe the isolation of a novel strain of HSV-1, and its engineering to safely harness it as an oncolytic therapeutic. This strain (UT1a) was isolated from a de-identified consented patient biorepository. CRISPR-Cas9-based recombination was utilized to insert bacterial artificial chromosome (BAC) genes into the viral UL39 and UL40 locus resulting in the deletion of both large and small subunits of the viral ribonucleotide reductase (RR). Subsequent deletion of viral RL1 genes encoding the neurovirulence factor ɣ34.5, resulted in OncoDelta (OncoD), a virus deleted for UL39, UL40 and both copies of RL1. OncoD retained tumor cell specific cytotoxicity and replication, was safe and non-toxic in intracranial injections in naïve mice up to doses of (5 x 106), maximal injectable dose OncoD and showed significant anti-tumor immune activating potential in multiple tumor models. Transcriptome profiling of OncoD showed that it impaired DNA damage repair pathways and hence synergized with radiation to improve therapeutic response in vitro and in vivo.

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Engineering a novel HSV-1 strain for oncolytic therapy of solid tumors

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A Combination of Chemotherapy and Oncolytic Virotherapy Sensitizes Colorectal Adenocarcinoma to Immune Checkpoint Inhibitors in a cDC1-Dependent Manner

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