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The LncRNA promotes vessel co-option mediated antiagiogenic therapies (AATs) resistance

ABSTRACT: The LncRNA promotes vessel co-option mediated antiagiogenic therapies (AATs) resistance

PROVIDER: PRJNA914872 | ENA |

REPOSITORIES: ENA

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Single cell transcriptomics profiling of vessel co-option

Project description:Vessel co-option is an alternative mode of tumor vascularization, which contributes to resistance to anti-angiogenic therapy (AAT). In contrast to vessel sprouting (angiogenesis), knowledge about the mechanisms underlying vessel co-option is minimal, precluding therapeutic strategies. We therefore single-cell RNA-sequenced 31,964 cells from a murine lung metastasis model with vessel co-option, characterized by resistance to AAT. Unexpectedly, co-opted endothelial cells (ECs) were transcriptomically indistinguishable from healthy ECs and lacked an activation signature, while co-opted pericytes expressed a quiescence signature, in contrast to activated pericytes during angiogenesis. Compared with cancer cells during angiogenesis, co-opting cancer cells were phenotypically more diverse and enriched in invasive subpopulations. Together, these data reveal new insight into vessel co-option, with possible implications for the development of therapeutic targets.

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Project description:To identify the lncRNAs that may participate in antiangiogenic therapy (AAT) resistance, the bevacizumab-resistant HCT116 CRCLM xenografts were established.

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Glioblastoma vessel co-option occurs as a resistance mechanism to chemoradiation via induction of a persister cell state

Project description:Glioblastoma (GB) is one of the deadliest types of human cancer. Recurrence after chemoradiation is mostly caused by regrowth of highly invasive and resistant cells. There is an urgent need to better understand the underlying GB mechanisms of chemoradiation resistance and tumor spreading. Using a combination of transcriptomic analysis, longitudinal imaging, organotypic cultures, functional assays, animal studies and clinical data analyses, we demonstrated that chemoradiation and brain vasculature induce a transition to an invasive functional cell state that we named VC-Resist. Better cell survival, G2M-arrest, senescence/stemness pathways’ induction and YAP activation make this GB cell state more resistant to therapy. Notably, these persister GB cells are highly vessel co-opting, allowing homing to the perivascular niche, which in turn increases their transition to this cell state. These findings demonstrate how vessel co-option, the perivascular niche, and GB cell plasticity jointly drive resistance during GB recurrence.

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Large scale transposon co-option in the Caenorhabditis germline regulatory network [longCapSeq]

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