ArticleBMC cancer2026
The role of PLOD family genes in liver hepatocellular carcinoma: from mechanisms to therapeutic potential.
Article in BMC cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Prognostic and therapeutic implications of PSMD14 in hepatocellular carcinoma: an integrative analysis of transcriptomic and single-cell profiles.Translational cancer research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLiver hepatocellular carcinoma (LIHC) is one of the most common and aggressive malignancies worldwide, with high mortality rates. PLOD family genes (PLOD1, PLOD2, and PLOD3) play a pivotal role in extracellular matrix (ECM) remodeling, which contributes to cancer progression and metastasis. This study explores the diagnostic, prognostic, and therapeutic potential of PLOD1, PLOD2, and PLOD3 in LIHC. MATERIALS AND
methodsSeven LIHC cell lines and five normal liver tissue cell lines were cultured. RT-qPCR was used to assess the expression of PLOD genes. The GSCA and TCGA databases were used for gene expression, pathway analysis, survival, and enrichment analysis. Promoter methylation was analyzed via GSCA and OncoDB, and mutational and CNV analyses were conducted using the cBioPortal database. The KM plotter tool assessed the prognostic significance of PLOD genes, while miRNA-mRNA network analysis was performed using the mirNET and UALCAN databases. Functional assays, including siRNA-mediated knockdown, Western blotting, cell proliferation, colony formation, and wound healing assays, were used to assess the biological roles of PLOD2 and PLOD3 in LIHC.
resultsThe expression of PLOD1, PLOD2, and PLOD3 was significantly (p-value < 0.05) higher in LIHC cell lines compared to normal controls. Validation in the TCGA cohort confirmed upregulation of PLOD genes in LIHC tumors, with PLOD2 and PLOD3 showing progressively higher expression across pathological stages. PLOD genes were associated with the activation of oncogenic pathways such as epithelial-to-mesenchymal transition (EMT) and poor survival outcomes. Promoter methylation analysis revealed lower methylation in tumor samples. Kaplan-Meier survival analysis indicated that higher PLOD expression correlated with poorer overall survival (OS) and relapse-free survival (RFS) in LIHC patients. The miRNA-mRNA network identified three miRNAs (hsa-miR-503-5p, hsa-miR-195-5p, and hsa-miR-193a-3p) regulating PLOD genes, with aberrant miRNA expression linked to poor prognosis. PLOD2/3 knockdown in HepG2 and Hep3B cells significantly reduced cell proliferation, colony formation, and migration, highlighting their critical roles in tumor progression.
conclusionOur study demonstrates that PLOD1, PLOD2, and PLOD3 are significantly upregulated in LIHC and correlate with poor prognosis. The PLOD genes may serve as valuable biomarkers for diagnosis and prognosis in LIHC. Moreover, targeting PLOD genes could provide new therapeutic strategies to hinder tumor progression and metastasis in liver cancer.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.