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Enhancing oncolytic virotherapy by extracellular vesicle mediated microRNA reprograming of the tumour microenvironment.

ABSTRACT: Enhancing oncolytic virotherapy by extracellular vesicle mediated microRNA reprograming of the tumour microenvironment.

PROVIDER: PRJNA1198511 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31721174.fastq.gz	Fastqsanger.gz
	SRR31721175.fastq.gz	Fastqsanger.gz
	SRR31721176.fastq.gz	Fastqsanger.gz
	SRR31721177.fastq.gz	Fastqsanger.gz
	SRR31721178.fastq.gz	Fastqsanger.gz

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Enhancing oncolytic virotherapy by extracellular vesicle mediated microRNA reprograming of the tumour microenvironment.

Project description:miRNA expression is critical in driving macrophage polarisation by simultaneously regulating expression of multiple cellular targets. Reintroducing miRNA to promote an anti-tumour macrophage phenotype is a promising therapeutic approach to reverse the immunosuppressive function of tumour associated macrophages.Small RNA sequencing was used to identify differentially expressed miRNA during TAM generation and following LPS/IFNγ stimulation to induce an anti-tumour phenotype. Two differentially expressed miRNA identified, miR-155 and miR-19a, were cloned into oncolytic rhabdovirus (ORV), and anti-tumour efficacy was investigated using both in vitro and in vivo models of OvCa.

2025-01-15 | GSE284314 | GEO

Pevonedistat sensitizes cancer cells to oncolytic VSVd51 virotherapy

Project description:Pevonedistat sensitizes cancer cells to oncolytic VSVd51 virotherapy

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T cell phenotype changes associated with oncolytic virotherapy combined with Nivolumab

Project description:There is a critical unmet need for safe and efficacious neoadjuvant treatment for cisplatin-ineligible patients with muscle invasive bladder cancer. We launched a Phase 1b study using the combination of intravesical cretostimogene grenadenorepvec (oncolytic serotype 5 adenovirus encoding granulocyte-macrophage colony stimulating factor) with systemic nivolumab in cisplatin-ineligible patients with cT2-4aN0-1M0 muscle invasive bladder cancer. The primary objective was to measure safety and the secondary objective to assess the antitumor efficacy of the combination. No dose limiting toxicity was encountered in 21 patients enrolled and treated. Combination treatment achieved a pathologic complete response rate of 42.1%, which was associated with baseline free E2F activity and tumor mutational burden, but not PD-L1 status. Although T cell infiltration was broadly induced following intravesical oncolytic virotherapy, the formation, enlargement and maturation of tertiary lymphoid structures (TLS) was specifically associated with complete response, supporting the importance of coordinated humoral and cellular immune responses. Together, these results highlight the potential of this combination regimen to enhance therapeutic efficacy in cisplatin-ineligible patients with muscle invasive bladder cancer, warranting its additional study as a neoadjuvant therapeutic option.

2025-09-04 | GSE276366 | GEO

Subclone of resistant CT26 murine tumor shows high sensitivity to VA7 virotherapy: A novel system to study innate immunity and antigen dominance in oncolytic immuno-virotherapy

Project description:Recently, attenuated Semliki Forest virus vector VA7 completely eliminated type I interferon (IFN) unresponsive human U87 glioma xenografts while IFN responsive mouse GL261 and CT-2A gliomas proved refractory to the oncolytic virotherapy. Here we describe in two clones of a well established Balb/c mouse tumor cell line, CT26 murine colon carcinoma, diametrically opposed IFN responsiveness and sensitivity to oncolytic virus. Both CT26WT and CT26LacZ clones secreted biologically active type I IFN in vitro upon infection but virus replication was self-limiting only in CT26WT cells. Total transcriptome sequencing (RNA-Seq) and western blotting experiments revealed that in sharp contrast to CT26LacZ cells, CT26WT cells had strong constitutive expression of 56 different genes associated with pattern recognition and type I interferon signaling pathways, spanning two reported anti-RNA virus gene signatures and22 genes that have been reported to have direct anti-Alphaviral activity. Correspondingly, only CT26LacZ tumors were infectable in vivo, resulting in rapid central necrosis of the tumors by 96 hours post infection and complete tumor eradication both in immunocompetent and in SCID mice. CT26LacZ tumor eradication by oncolysis induced 100% protective immunity against homologous CT26LacZ challenge but only 50% protection against heterologous CT26WT challenge, indicating LacZ immune dominance over shared antigens. We believe the two clone CT26 system described herein constitutes a challenging yet realistic model for clonally and immunologically heterogeneous cancer where a strong therapy efficacy bias toward sensitive tumor subpopulations might falsely predict therapeutic success on a broad patient scale highlighting the necessity of successful pre-screening for responsive tumors. RNA-Seq in CT26 tumor cell line

2014-09-05 | E-GEOD-53001 | biostudies-arrayexpress

Reprograming responsiveness of tolerogenic CD8+ T cells using a CXCR4 antagonist-armed oncolytic virus requires reversal of M2 macrophage polarization

Project description:Overcoming barriers to the generation of antitumor immunity to self-and neo-antigens is a central concern of cancer immunotherapy. This study investigated the effect of interactions between ovarian cancer (OC) cells and the tumor microenvironment (TME) on the ability of oncolytic virotherapy to activate responsiveness of self antigen-specific and neoantigen-specific CD8+ T lymphocytes in tolerogenic and wild-type (WT) murine tumor models, respectively

2022-06-30 | GSE199880 | GEO

Pevonedistat sensitizes cancer cells to oncolytic VSVd51 virotherapy

Project description:To investigate the ability for pevonedistat to sensitize renal 786-0 carcinoma cells to VSVd51 oncolyic virotherapy, we treated cells with monotherapies or combination and sequencinced the transcriptome for antiviral interferon impact

2023-09-28 | GSE206428 | GEO

T cell phenotype changes associated with oncolytic virotherapy combined with Nivolumab

Project description:T cell phenotype changes associated with oncolytic virotherapy combined with Nivolumab

| PRJNA1156788 | ENA

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.

2021-10-31 | GSE186753 | GEO

Itaconate enhances oncolytic virotherapy via multitarget inhibition of antiviral and inflammatory pathways

Project description:Itaconate enhances oncolytic virotherapy via multitarget inhibition of antiviral and inflammatory pathways

| PRJNA972486 | ENA

ZIKV infection series in paediaitric brain tumour and NPC cell lines

Project description:Zika virus (ZIKV) is a mosquito-borne flavivirus consisting of historical African and epidemic-associated Asian lineages. The latter can access the central nervous system and causes microcephaly in the developing foetus through infection and depletion of neural stem and progenitor cells. The molecular mechanisms involved in this depletion response are grossly unknown for cells arising from CZS-affected children. Since 2017, the concept of employing ZIKV as oncolytic virotherapy against brain tumours has gained momentum. Oncolytic virotherapy exploits viruses that preferentially infect and destroy cancer cells via two distinct routes of therapeutic action. Following infection, intense viral replication induces oncolysis, releasing virions into the tumour microenvironment to infect neighbouring tumour cells. ZIKV induces an oncolytic event in infected pediatric brain tumour cells, but the molecular mechanisms involved in this response are grossly unknown. Here, we sought to investigate the molecular mechanisms underlying both the oncolytic and neuropathogenic responses of ZIKV infection in brain tumour and NPCs, respectively.

2025-04-23 | GSE277900 | GEO

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