ArticleMolecular and cellular biochemistry2022
PLOD1 acts as a tumor promoter in glioma via activation of the HSF1 signaling pathway.
Article in Molecular and cellular biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Integrated Analysis of Proteomics and Metabolomics for Heat Stress in Chinese Holstein Cows.Animals : an open access journal from MDPI · 2025Article
- Prognostic biomarker and clinical significance of PLOD gene family in clear cell renal cell carcinoma.Frontiers in oncology · 2025Article
- Comprehensive Analysis of the Expression, Prognosis, and Biological Significance of PLOD Family in Bladder Cancer.International journal of general medicine · 2023Article
- Identification and characterization of putative biomarkers and therapeutic axis in Glioblastoma multiforme microenvironment.Frontiers in cell and developmental biology · 2023Article
- The Inflamm-Aging Model Identifies Key Risk Factors in Atherosclerosis.Frontiers in genetics · 2022Article
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3 authors.
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Abstract
Procollagen-lysine, 2-oxoglutarate 5-dioxygenase 1 (PLOD1) is a collagen-related lysyl hydroxylase and its prognostic value in glioma patients was verified. However, its biological function in glioma has yet to be fully investigated. The PLOD1 mRNA status and clinical significance in gliomas were assessed via the GEPIA database. Overexpression or targeted depletion of PLOD1 was carried out in the human glioma cell line U87 and verified by western blotting. CCK8 and colony formation assays were implemented to examine the impact of PLOD1 on the proliferative and colony-forming phenotypes of U87 cells. Luciferase reporter assays and HSF1-specific pharmacologic inhibitors (KRIBB11) were employed to determine the regulatory relationship between PLOD1 and heat shock factor 1 (HSF1). High expression of PLOD1 was observed in tissue samples of glioblastoma multiforme (GBM) and brain lower-grade glioma (LGG). GEPIA overall survival further demonstrated that both GBM and LGG patients with high PLOD1 displayed worse clinical outcomes compared with those with low PLOD1. Overexpression and targeted depletion of PLOD1 enhanced and suppressed U87 cell proliferation and colony formation, respectively. Luciferase reporter assays showed that PLOD1 significantly enhanced the transcriptional activity of HSF1 in HEK293T cells. PLOD1 deficiency in U87 cells inhibited HSF1-induced survivin accumulation, whereas KRIBB11 also blocked the PLOD1-overexpressing induced survivin expression. An inhibitor of HSF1 signaling events abolished the increased clonogenic potential caused by PLOD1 overexpression in U87 cells. High expression of PLOD1 can increase the proliferation and colony formation of U87 cells by activating the HSF1 signaling pathway. This study suggested PLOD1/HSF1 as an effective therapeutic target for gliomas.
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