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Radiation-induced amphiregulin drives tumor metastases

ABSTRACT: Radiation-induced amphiregulin drives tumor metastases

PROVIDER: PRJNA1053776 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27237225.fastq.gz	Fastqsanger.gz
	SRR27237226.fastq.gz	Fastqsanger.gz
	SRR27237227.fastq.gz	Fastqsanger.gz
	SRR27237228.fastq.gz	Fastqsanger.gz
	SRR27237229.fastq.gz	Fastqsanger.gz

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Radiation-induced amphiregulin drives tumor metastasis

Project description:Radiation-induced amphiregulin drives tumor metastasis

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Radiation-induced amphiregulin drives tumor metastases

Project description:In this study, we demonstrate that radiation induces the epidermal growth factor receptor (EGFR) ligand amphiregulin (AREG) in tumor cells, which stimulates distant metastasis proliferation in both patients and pre-clinical murine tumor models. Using single-cell RNAseq (sc-RNAseq), we characterized the effects of AREG-induction on immune cells in the lung metastatic microenvironment of B6 mice.

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Radiation-induced amphiregulin drives tumor metastasis

Project description:The anti-tumor effect of radiotherapy (RT) beyond the treatment field - the abscopal effect - has garnered much interest. By contrast, the potentially harmful impact of radiation in promoting metastasis is less well studied. Here, we show that RT induces the expression of epidermal growth factor receptor (EGFR) ligand amphiregulin (AREG) in tumor cells, which reprograms EGFR+ myeloid cells toward an immunosuppressive phenotype and reduces phagocytosis. This stimulates distant metastasis growth in both patients and pre-clinical murine tumor models. The inhibition of these tumor-promoting factors induced by RT may represent a novel therapeutic strategy to improve patient outcomes.

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Project description:Numerous case studies have reported spontaneous regression of metastases following tumor excision, but underlying mechanisms are elusive. Here we present a model of metastases regression and latency elicited by the removal of a primary tumor, and identify underlying mechanisms. Human breast cancer cells, expressing highly sensitive luciferase, were implanted into the mammary fat-pad of mice, and the progression of early stage micrometastases, was monitored. Upon establishment of micrometastases, the primary tumor was excised, inducing a robust regression of metastatic signal, resulting in latent foci. In vivo supplementation of tumor secretome immediately upon tumor excision diminished this regression, implicating primary tumor secreted factors in promotion of metastatic growth. In vitro, cancer cell conditioned medium reduced apoptosis and enhanced adhesion of non-confluent cancer cells, and induced angiogenesis in endothelial cells. Cytokine array and proteomic analysis of cancer cells secretome identified 359 extracellular secreted factors, with significant enrichment of angiogenic factors, growth factors activity, focal adhesion, apoptosis, and metalloprotease processes. In vivo blockade of four key potential mediators of these processes, IL-8, PDGFaa, Serpin E1 (PAI-1), and MIF, arrested development of micrometastases. Moreover, high protein levels of these four factors were correlated with poor patient outcome. These results demonstrate regression and latency of metastases following tumor excision and a crucial role for primary tumor secretome in promoting early metastatic stages, suggesting novel mechanisms to control minimal residual disease.

2020-10-07 | PXD008384 | Pride

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Project description:Transcriptional profiling of transgenic mice specifically expressing amphiregulin in white adipose tissues. The objective of this study is to explore gene expression profiles of adipose tissues in response to amphiregulin overexpression.

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The tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway Phospho

Project description:Phosphoproteomics show that the tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING-IFNb pathway

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Project description:Jailkhani N, Clauser KR, Mak H, Rickelt S, Tian C, Whittaker CA, Tanabe KK, Purdy SR, Carr SA, and Hynes RO.2022. Metastases are hard to detect and treat, and cause most cancer-related deaths. The relative lack of therapies targeting metastases represents a major unmet clinical need. The extracellular matrix or ECM forms a major component of the tumor microenvironment in both primary and metastatic tumors and certain ECM proteins can be selectively and abundantly expressed in such tumors. We propose that nanobodies against ECM proteins that show selective abundance in metastases can be used as vehicles for delivery of imaging and therapeutic cargoes. To gain a deeper understanding of the microenvironment of human metastases, we describe here an LC-MS/MS-based ECM signature shared by human TNBC and CRC metastases to different organs and provide evidence that this conserved set of ECM proteins is selectively elevated in other tumors. We also describe phage-display libraries of nanobodies raised against ECM-enriched preparations from human metastases from TNBC and CRC. As proof of concept, we developed selective and specific, high-affinity nanobodies against an example signature protein, Tenascin-C (TNC), known to be abundant in many tumor types and to play a role in metastases. We report that TNC is abundantly expressed in patient metastases and widely expressed across diverse metastatic sites originating from several primary tumor types. Using immuno-PET/CT we showed that anti-TNC nanobodies bind TNBC tumors and metastases with excellent specificity. We propose that such generic anti-tumor nanobodies are promising cancer-agnostic, in vivo tools for the delivery of therapeutics to tumor and metastatic ECM.

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