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Targeted release of a bispecific fusion protein SIRPα/Siglec-10 by oncolytic adenovirus reinvigorates tumor associated macrophages to improve therapeutic outcomes in solid tumors

ABSTRACT: Targeted release of a bispecific fusion protein SIRPα/Siglec-10 by oncolytic adenovirus reinvigorates tumor associated macrophages to improve therapeutic outcomes in solid tumors

PROVIDER: PRJNA1153574 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30442907_1.fastq.gz	Fastqsanger.gz
	SRR30442907_2.fastq.gz	Fastqsanger.gz
	SRR30442908_1.fastq.gz	Fastqsanger.gz
	SRR30442908_2.fastq.gz	Fastqsanger.gz
	SRR30442909_1.fastq.gz	Fastqsanger.gz

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Targeted release of a bispecific fusion protein SIRPα/Siglec-10 by oncolytic adenovirus reinvigorates tumor associated macrophages to improve therapeutic outcomes in solid tumors

Project description:CD47/SIRPα and CD24/Siglec-10 signaling pathways have been found to suppress macrophage phagocytosis of malignant cells. We constructed a recombinant oncolytic adenovirus expressing a fusion protein composed of the extracellular domains of murine SIRPα and Siglec-10 (SIRPα/Siglec-10), termed AdV-mSS. Intratumoral administration of AdV-SS markedly enhanced antitumor efficacy than AdV-Ctrl in multiple solid tumor models. To reveal differences in biological processes between them. subcutaneous 14-day H22-CAR -bearing BALB/c mice were intratumorally injected with PBS, 5 × 10^8 IFU AdV-Ctrl, or 5 × 10^8 IFU AdV-mSS twice. Forty-eight hours post-treatment, we harvested tumor tissue and sorted these TAMs by anti-mouse F4/80 magnetic beads. Samples were subjected to transcriptome sequencing.

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Thymosin α1 reverses oncolytic adenovirus-induced M2 polarization of macrophages to improve antitumor immunity and therapeutic efficacy

Project description:Although oncolytic adenoviruses have been widely studied for their direct oncolytic activity and immunomodulatory role in cancer immunotherapy, the immunosuppressive feedback loop induced by oncolytic adenoviruses remains poorly studied. Here, we showed that type V adenovirus (ADV) induces the polarization of tumor-associated macrophages (TAMs) to the M2 phenotype and increases the infiltration of regulatory T cells (Tregs) in the tumor microenvironment (TME). By selectively compensating for these deficiencies, Tα1 reprogrammed “M2-like” TAMs toward an antitumoral phenotype, thereby reprogramming the TME into a state more beneficial for antitumor immunity. Moreover, ADVTα1 was constructed by harnessing the merits of all the components for the aforementioned combinatorial therapy. Both in vitro and in vivo data showed that both exogenously supplied and adenovirus-produced Tα1 orchestrate TAM reprogramming and enhance the antitumor efficacy of ADV via CD8+ T cells, showing promising prospects for clinical translation. Our findings provide inspiration for improving oncolytic adenovirus combination therapy and designing new oncolytic engineered adenoviruses.

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Project description:The microtubule-stabilising drug paclitaxel has activity in relapsed ovarian cancer. However, resistance frequently develops. Oncolytic adenoviruses are a novel cancer therapy, and replicate selectively within and lyse malignant cells, leading to productive infection of neighbouring cells. We found increased efficacy of adenoviruses of multiple subtypes in paclitaxel-resistant ovarian cancer cells. There was increased expression of a key adenovirus receptor, CAR (coxsackie adenovirus receptor), due to increased transcription that resulted from histone modification. Moreover, CAR transcription increased in intraperitoneal xenografts with acquired paclitaxel resistance and in tumours from patients with paclitaxel-resistant ovarian cancer. Finally, we identified dysregulated cell cycle control as a second mechanism of increased adenovirus efficacy in paclitaxel-resistant ovarian cancer and that inhibition of CDK4/6 using PD-0332991 was able both to reverse paclitaxel resistance and reduce adenovirus efficacy. Thus, paclitaxel resistance increases oncolytic adenovirus efficacy via at least two separate mechanisms. Parental SKOV3 and paclitaxel-resistant SKOV3-TR cells were analysed in duplicate

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nuclear proteomics of glioma cells infected with an oncolytic adenovirus

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