ArticleCancer research communications2026
Vitronectin Enrichment in Prostate Cancer Liver Metastases Promotes Adhesion and Survival.
Article in Cancer research communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The development of liver metastases in prostate cancer is associated with aggressive disease and poor prognosis. Because hepatocytes exhibit high metabolic activity with unique secretory profiles, we hypothesized that hepatocyte-to-tumor cell signaling plays a role in promoting liver metastasis. We evaluated single-cell transcriptomic data and metastatic tissue from patients with castration-resistant prostate cancer spanning androgen receptor (AR)-positive and AR-negative pathologies. Despite extensive intra- and intersample heterogeneity, communication analysis predicted vitronectin (VTN) engagement of tumor integrins as a common feature. VTN-positive hepatocytes were observed in prostate tumors with VTN accumulation in sinusoidal patches. Consistent with integrin activation, VTN treatment of AR-positive and AR-negative prostate cancer cells significantly promoted tumor cell adhesion, inhibited hypodiploid accumulation in accordance with survival effects, and stimulated FAK-dependent phosphorylation of ERK and AKT. FAK inhibition with defactinib abrogated VTN- and serum-mediated adhesion in a cell-specific manner and mitigated VTN-driven depletion of hypodiploid populations. These findings support a model in which dense intrasinusoidal VTN deposits capture metastatic prostate tumor cells in the liver and biochemically activate tumorigenic signaling, promoting tumor aggressiveness. SIGNIFICANCE: Through the synthesis of single-cell transcriptomic data with experimental models, we identify VTN as a candidate microenvironmental mediator of prostate cancer liver colonization. VTN drives cell adhesion, inhibits hypodiploid accumulation consistent with cell survival, and activates oncogenic signaling, which may be inhibited by the dual FAK/PYK2 inhibitor defactinib.
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