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Effect of QPRT overexpression on gene expression in cancer pericyte cells

ABSTRACT: Cancer pericytes are core components of the tumor microenvironment, governing tumor angiogenesis, invasion, and therapeutic resistance; QPRT (quinolinic acid phosphoribosyltransferase), a key metabolic enzyme, is implicated in modulating cellular metabolic homeostasis and malignant progression. We here investigate the transcriptomic impact of QPRT overexpression in cancer pericyte cells. QPRT overexpression induces widespread alterations in gene expression profiles, with dysregulated genes predominantly enriched in pathways related to tumor-associated angiogenesis, pericyte activation, and cell-matrix adhesion. Functional characterization shows that QPRT overexpression upregulates pro-angiogenic factors (e.g., VEGF, PDGF-BB) and adhesion molecules, enhancing the paracrine regulatory capacity of cancer pericytes on adjacent tumor vasculature. Mechanistically, QPRT-mediated metabolic reprogramming contributes to the activation of these pro-tumorigenic pathways. Taken together, our data reveal a critical role of QPRT overexpression in remodeling the transcriptome of cancer pericyte cells, providing insights into metabolic modulation of tumor microenvironment function.

ORGANISM(S): Homo sapiens

PROVIDER: GSE312849 | GEO | 2025/12/31

REPOSITORIES: GEO

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Project description:Background: Pericytes regulate vessel stabilization and function and their loss is associated with diseases such as diabetic retinopathy or cancer. Despite their physiological importance, pericyte function and molecular regulation during angiogenesis remain poorly understood. Methods: To decipher the transcriptomic programs of pericytes during angiogenesis, we crossed the Pdgfrb(BAC)-CreERT2 into the RiboTagflox/flox mice. Pericyte morphological changes were assessed in mural cell-specific R26-mTmG reporter mice, in which low doses of tamoxifen allowed labeling of single cell pericytes at high resolution. To study the role of phosphoinositide 3-kinase (PI3K) signaling in pericyte biology during angiogenesis, we used genetic mouse models which allow selective inactivation of PI3Kα and PI3Kβ isoforms and their negative regulator PTEN (phosphate and tensin homologue deleted on chromosome ten, PTEN) in mural cells. Results: At the onset of angiogenesis, pericytes exhibit molecular traits of cell proliferation and activated PI3K signaling, whereas during vascular remodeling pericytes upregulate genes involved in mature pericyte cell function, together with a remarkable decrease in PI3K signaling. Immature pericytes showed stellate shape and high proliferation, and mature pericytes were quiescent and elongated. Unexpectedly, we demonstrate that the PI3Kβ, but not PI3Kα, regulates pericyte proliferation and maturation during vessel formation. Genetic PI3Kβ inactivation in pericytes triggered early pericyte maturation. Conversely, unleashing PI3K signaling by means of PTEN deletion delayed pericyte maturation. Pericyte maturation was necessary to undergo vessel remodeling during angiogenesis. Conclusions: Our results identify new molecular and morphological traits associated to pericyte maturation and uncover PI3Kβ activity as a checkpoint to ensure appropriate vessel formation. In turn, our results may open new therapeutic opportunities to regulate angiogenesis in pathological processes through the manipulation of pericyte PI3Kβ activity.

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Effect of QPRT overexpression on gene expression in cancer pericyte cells

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