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Extracellular acidosis promotes colonization of lung metastases by mediating extracellular matrix remodeling and vasculogenic mimicry

ABSTRACT: Extracellular acidosis promotes colonization of lung metastases by mediating extracellular matrix remodeling and vasculogenic mimicry

PROVIDER: PRJNA825255 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18700906_1.fastq.gz	Fastqsanger.gz
	SRR18700906_2.fastq.gz	Fastqsanger.gz
	SRR18700907_1.fastq.gz	Fastqsanger.gz
	SRR18700907_2.fastq.gz	Fastqsanger.gz
	SRR18700908_1.fastq.gz	Fastqsanger.gz

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Extracellular acidosis promotes colonization of lung metastases by mediating extracellular matrix remodeling and vasculogenic mimicry

Project description:Acidosis is a hallmark of the tumor microenvironment caused by the metabolic switch from glucose oxidative phosphorylation to glycolysis. It has been largely associated with tumor growth and progression, nevertheless, how acidosis promotes metastatic dissemination remains largely unknown. In this study, we established a long-term acidosis model using patient-derived lung cancer cells. By comparing xenograft inoculates at the cluster sizes of lung cancer circulating tumor cells, the acidosis cells display significantly higher incidence of secondary tumor establishment than their neutral pH counterparts. Transcriptomics analyses reveal a profound remodeling of the extracellular matrix in the acidosis cells, featuring the upregulation of ITGA4 and HAS3 genes, In clinical specimen, overexpression of both ITGA4 and HAS3 proteins are associated with primary tumors with metastatic ability, and their distribution is markedly accentuated around vascular mimicry structures in secondary tumors. We show that acidosis cells display higher ability of vascular mimicry in vitro, and are enriched in ABC transporter-dependent side population cells. Our data support that acidosis drives tumor metastatic colonization via enhanced extracellular matrix remodeling and vascular mimicry. Assessment on the prognostic value of tumor acidosis for metastasis and possible treatment directions are discussed.

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Gene expression of osteosarcama cell line with vasculogenic mimicry phenotype

Project description:Vasculogenic mimicry has been generally accepted as a new form of tumor vascularization and regarded as an unfavorable prognostic factor in multiple aggressive malignancies. We previously reported the presence of vasculogenic mimicry in osteosarcoma patients. The mechanistic basis for osteosarcoma VM remains unclear. We used microarrays to detail the global programme of gene expression between 143B cells and HOS cells exposed to Matrigel which showed greatly different vasculogenic mimicry formation potential and identified distinct classes of vasculogenic mimicry-realted genes during this process.

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An interplay between extracellular matrix proteins and the cancer cell promotes the multistep process of in vitro vasculogenic mimicry formation.

Project description:Cancer vasculogenic mimicry (VM) is the formation of vasculature structures in the absence of endothelial cells. We previously established an in vitro model that facilitates the formation of a lumen-containing and fluid-conducting tubular structures after 4 days cancer cell growth on Matrigel. Herein, we mechanistically characterize this model in breast and ovarian cancer cell lines demonstrating distinct phases of VM formation and the dependence of specific extracellular matrix proteins. We report that VM occurs in four distinct stages. Firstly, alignment, migration then clustering delineate the area of the future tubular structure. Secondly, contraction of aligned structures followed by loss of attachment of some cells and cellular blebbing. Thirdly, a phase of mass proliferation followed by the raising of specific areas of the cancer cell mass above the Matrigel (bridge). Finally, the formation of a cell monolayer closes the tubular structure, forms a glycoprotein-rich luminal lining, then elevates the structure. Only later stages of VM require AKT and FAK signaling. We demonstrate that the lining of the tubular lumen is rich in laminin. Laminin 111 (but not collagen I) must be presence in the extracellular matrix (Matrigel) for VM to occur and integrin β1, but not integrin β3, is required. RNASeq demonstrates that formation is principally post-transcriptional regulation, however, this technique together with siRNA knockdown identified the first and essential biological function for the protein SMIM11A. VM is associated with poor patient survival and thus an understanding of the mechanism of VM may bring to light novel anticancer targets.

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