ArticleApplied biochemistry and biotechnology2026
PROK1 Induces Macrophage M2 Phenotype Conversion to Promote Pancreatic Cancer Progression by Activating the PI3K/AKT Pathway Via Interacting with PROKR2.
Article in Applied biochemistry and biotechnology, 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 impact and mechanisms of PROK1 on macrophages in pancreatic cancer (PC) progression was investigated. PROK1 and PROKR2 expression in PC patients were detected by immunohistochemistry and Western blot. TIMER database analyzed correlation between PROK1/PROKR2 and macrophage infiltration in PC. PROK1 influence on macrophage M2 phenotypic conversion and PI3K/AKT pathway activity were investigated by detecting CD206, IL-10, Arg-1, p-PI3K/PI3K and p-AKT/AKT via immunofluorescence and Western blot. PROK1 in macrophages on viability, migration and invasion of PC cells was appraised by CCK-8, wound healing and Transwell assays. Immunoprecipitation verified the interaction between PROK1 and PROKR2. Western blot explored regulation of PROK1 and PROKR2 on PI3K/AKT pathway activity and macrophage M2 phenotypic conversion. In vivo study was executed by constructing xenograft tumor models. PROK1 and PROKR2 overexpression in PC patients was associated with macrophage infiltration, advanced TNM stage, lymph node and distant metastasis. PROK1 silencing suppressed macrophage M2 phenotypic conversion and PI3K/AKT pathway activity, as it reduced CD206, IL-10, Arg-1, p-PI3K/PI3K, and p-AKT/AKT. PROK1 silencing in M2 macrophages attenuated PC cell viability, migration and invasion. PROK1 interacted with PROKR2 to activate PI3K/AKT pathway in macrophages. PROK1 elevated CD206, IL-10 and Arg-1 in M2 macrophages, which was reversed by PROKR2 silencing. In vivo, PROK1 in macrophages enhanced PC growth and expression of CD206, IL-10, Arg-1, p-PI3K/PI3K and p-AKT/AKT in xenograft tumors, which was abrogated by PROKR2 silencing. PROK1 induced macrophage M2 phenotype conversion to promote PC progression by activating the PI3K/AKT pathway via interacting with PROKR2.
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