ArticleBJC reports2024
Targeting PLOD2 suppresses invasion and metastatic potential in radiorecurrent prostate cancer.
Article in BJC reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Plasma Proteins Associated with Whole Grains and Fiber Intake in the Cardiovascular Health Study (CHS) and the Atherosclerosis Risk in Communities (ARIC) Study.The Journal of nutrition · 2026Article
- LH2 Promotes Tumor Progression in Oral Squamous Cell Carcinoma via EPHA7-AKT-VEGF Signaling.Journal of Cancer · 2026Article
- Proteome-Wide Discovery of Degradable Proteins Using Bifunctional Molecules.ACS central science · 2025Article
- Accelerated growth and local progression of radiorecurrent prostate cancer in an orthotopic bioluminescent mouse model.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Background: Metastatic relapse of prostate cancer after radiotherapy is a significant cause of prostate cancer-related morbidity and mortality. PLOD2 is a mediator of invasion and metastasis that we identified as being upregulated in our highly aggressive radiorecurrent prostate cancer cell line. Methods: Patient dataset analysis was conducted using a variety of prostate cancer cohorts. Prostate cancer cell lines were treated with siRNA, or the drug PX-478 prior to in vitro invasion, migration, or in vivo chick embryo (CAM) extravasation assay. Protein levels were detected by western blot. For RNA analysis, RNA sequencing was conducted on PLOD2 knockdown cells and validated by qRT-PCR. Results: PLOD2 is a negative prognostic factor associated with biochemical relapse, driving invasion, migration, and extravasation in radiorecurrent prostate cancer. Mechanistically, HIF1α upregulation drives PLOD2 expression in our radiorecurrent prostate cancer cells, which is effectively inhibited by HIF1α inhibitor PX-478 to reduce invasion, migration, and extravasation. Finally, the long non-coding RNA LNCSRLR acts as a promoter of invasion downstream of PLOD2. Conclusions: Together, our results demonstrate for the first time the role of PLOD2 in radiorecurrent prostate cancer invasiveness, and point towards its potential as a therapeutic target to reduce metastasis and improve survival outcomes in prostate cancer patients.
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Registered trials
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