ArticleOncogene2021
Hypoxia-induced PLOD1 overexpression contributes to the malignant phenotype of glioblastoma via NF-κB signaling.
Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 61 citations in OpenAlex.
- PLOD1 Catalytic Activity Stabilizes ENO1 by Limiting FBXW7-dependent Degradation to Promote Glycolysis and TMZ Resistance in Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Extracellular Matrix Remodeling in Tumors: Forces Beyond Fibroblasts.Cancer research · 2026Article
- Lactate-induced H3K4me3 histone mark promotes PLOD1-driven prostate cancer invasion.Cell death & disease · 2026Article
- PLOD1 Drives Head and Neck Squamous Cell Carcinoma Progression Through P4HA2-Mediated Activation of the FAK/PI3K/AKT/mTOR Axis.Journal of cellular and molecular medicine · 2026Article
- CSRP2 modulates PDGFRA/PI3K/AKT signaling via PRC1 components in glioma.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Multi-omics evidence reveals a causal role of endoplasmic reticulum stress in cancer development.PeerJ · 2026Article
- Mass spectrometry-based multi-omics analysis elucidates immune microenvironmental characteristics and the risk of distant metastasis in N1c colorectal cancer.Frontiers in immunology · 2026Article
- Bioinformatic Approach to Identify Positive PrognosticInternational journal of molecular sciences · 2025Article
- Perfluorooctanesulfonamide-induced epiboly delay is associated with decreased ATP production within zebrafish embryos.Ecotoxicology and environmental safety · 2025Article
- PLOD1 promotes gastric cancer metastasis and immune escape by mediating extracellular matrix remodeling.Discover oncology · 2025Article
- Phenotypic variations in glioma stem cells: regulatory mechanisms and implications for therapeutic strategies.Journal of translational medicine · 2025Review
- PLOD1 promotes the malignancy of hepatocellular carcinoma by facilitating the NF-κB/IL-6/STAT3-dependent TCA cycle.JHEP reports : innovation in hepatology · 2025Article
- Hypomethylation induced overexpression of PLOD3 facilitates colorectal cancer progression through TM9SF4-mediated autophagy.Cell death & disease · 2025Article
- GNE-317 Reverses MSN-Mediated Proneural-to-Mesenchymal Transition and Suppresses Chemoradiotherapy Resistance in Glioblastoma via PI3K/mTOR.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- To investigate the tumor promotion role of PLOD3 in colorectal cancer and its potential as a prognostic biomarker and therapeutic target.Scientific reports · 2025Article
- Sesquiterpene Lactones as Promising Anti-Glioblastoma Drug Candidates Exerting Complex Effects on Glioblastoma Cell Viability and Proneural-Mesenchymal Transition.Biomedicines · 2025Review
- Prognostic biomarker and clinical significance of PLOD gene family in clear cell renal cell carcinoma.Frontiers in oncology · 2025Article
- CKAP4 and PLOD2 as novel prognostic biomarkers in hepatocellular carcinoma: a proteomics-driven risk stratification model.Frontiers in cell and developmental biology · 2025Article
- CCN1 Promotes Mesenchymal Phenotype Transition Through Activating NF-κB Signaling Pathway Regulated by S100A8 in Glioma Stem Cells.CNS neuroscience & therapeutics · 2024Article
- Comprehensive understanding of glioblastoma molecular phenotypes: classification, characteristics, and transition.Cancer biology & medicine · 2024Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Procollagen lysyl hydroxylase 1 (PLOD1) is highly expressed in malignant tumors such as esophageal squamous cell carcinoma, gastric cancer, and colorectal cancer. Bioinformatics analysis revealed that PLOD1 is associated with the progression of GBM, particularly the most malignant mesenchymal subtype (MES). Moreover, in the TCGA and CGGA datasets, the mean survival time of patients with high PLOD1 expression was significantly shorter than that of patients with low expression. The clinical samples confirmed this result. Therefore, we aimed to investigate the effect of PLOD1 on the development of mesenchymal GBM in vitro and in vivo and its possible mechanisms. Molecular experiments were conducted on the patient-derived glioma stem cells and found that PLOD1 expressed higher in tumor tissues and cancer cell lines of patients with GBM, especially in the MES. PLOD1 also enhanced tumor viability, proliferation, migration, and promoted MES transition while inhibited apoptosis. Tumor xenograft results also indicated that PLOD1 overexpression significantly promotes malignant behavior of tumors. Mechanistically, bioinformatics analysis further revealed that PLOD1 expression was closely associated with the NF-κB signaling pathway. Besides, we also found that hypoxic environments also enhanced the tumor-promoting effects of PLOD1. In conclusion, overexpression of PLOD1 may be an important factor in the enhanced invasiveness and MES transition of GBM. Thus, PLOD1 is a potential treatment target for mesenchymal GBM or even all GBM.
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