ArticleCancer genomics & proteomics
PPIL1 Drives Hepatocellular Carcinoma Progression and Cancer Stem Cell Self-renewal Through DAAM2-mediated Wnt/β-Catenin Activation.
Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- SPINT2 Is Associated with Dual-Phenotype Hepatocellular Carcinoma and Aggressive Tumor Features.Cancers · 2026Article
- PPIL1 promotes hepatocellular carcinoma progression and associates with poor prognosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimHepatocellular carcinoma (HCC) accounts for ~90% of primary liver cancer, which ranks as the third-leading cause of global cancer mortality. Emerging evidence establishes cancer stem cells (CSCs) as central regulators of HCC progression, metastasis, and therapeutic resistance, with stemness-related pathways like Wnt/β-catenin signaling critically maintaining CSC self-renewal. In this study, we aimed to investigate the role of Peptidyl-prolyl isomerase-like 1 (PPIL1) in HCC progression and CSC self-renewal. MATERIALS AND
methodsPPIL1 expression patterns were systematically analyzed using The Cancer Genome Atlas Liver Hepatocellular Carcinoma (TCGA-LIHC) data and validated in primary HCC specimens
resultsOur analysis revealed significantly elevated PPIL1 expression in HCC tumors and liver CSCs, with its expression level positively correlating with tumor stage and histological grade. PPIL1 knockdown effectively suppressed HCC cell proliferation, migration, and
conclusionOur findings suggest PPIL1 to be a crucial regulator of HCC progression and liver CSC maintenance
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