ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
PPIL1 promotes hepatocellular carcinoma progression and associates with poor prognosis.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 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
Peptidylprolyl isomerase like 1 (PPIL1) is a component of the Prp19 complex (Prp19C), which plays a crucial role in spliceosome assembly. However, the role of PPIL1 in hepatocellular carcinoma (HCC) progression remains unclear. Analysis of TCGA and LIRI-JP datasets revealed that elevated expression of components from the Prp19 complex (Prp19C) is associated with poor prognosis in HCC. PPIL1, which significantly exacerbated tumor progression in this complex, would be a promising therapy target. To investigate the effect of PPIL1 on HCC cells, CCK-8, colony formation, and sphere-formation assays were performed to evaluate its influence on proliferation. Wound healing and Transwell assays were conducted to assess migration and invasion capabilities. The results demonstrated that knockdown of PPIL1 significantly attenuated the malignant phenotype of HCC cells by reducing their capability for proliferation, as well as by diminishing their potential for migration, invasion, and stemness. Flow cytometry analysis demonstrated that PPIL1 knockdown induces G2/M phase cell cycle arrest in HCC cells. Western blot analysis showed that knockdown of PPIL1 significantly suppressed the mTOR/ERK/NF-κB signaling cascade and the expression of CHK2. Overall, our results demonstrated that PPIL1 is highly expressed in HCC tissues and is associated with poor prognosis. Functionally, PPIL1 drives the malignant phenotype of HCC cells and modulates the mTOR/ERK/NF-κB pathway and the expression of CHK2.
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