ArticleLaboratory investigation; a journal of technical methods and pathology2022
PLOD3 regulates the expression of YAP1 to affect the progression of non-small cell lung cancer via the PKCδ/CDK1/LIMD1 signaling pathway.
Article in Laboratory investigation; a journal of technical methods and pathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 8 citations in OpenAlex.
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- AJUBA promotes the proliferation, invasion and migration of NSCLC cells by activating the ERK/β-catenin pathway.Scientific reports · 2025Article
- Construction and validation of a prognostic model based on oxidative stress-related genes in non-small cell lung cancer (NSCLC): predicting patient outcomes and therapy responses.Translational lung cancer research · 2024Article
- Integrative analysis regarding the correlation between collagen-related genes and prostate cancer.BMC cancer · 2024Article
- RBM15 increase tumor-infiltrating CD4+ T cell in ESCCAmerican journal of cancer research · 2024Article
- Identification of PLOD3 and LRRN3 as potential biomarkers for Parkinson's disease based on integrative analysis.NPJ Parkinson's disease · 2023Article
- Diagnostic, Prognostic, and Immunological Roles of HELLS in Pan-Cancer: A Bioinformatics Analysis.Frontiers in immunology · 2022Article
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6 authors at 1 institution in 1 country.
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Abstract
Procollagen-lysine, 2-oxoglutarate 5-dioxygenase (PLOD3) is a crucial oncogene in human lung cancer, whereas protein kinase C δ (PKCδ) acts as a tumor suppressor. In this study, we aimed to explore the regulation by PLOD3 on the expression of YAP1 to affect the progression of non-small cell lung cancer (NSCLC) via the PKCδ/CDK1/LIMD1 signaling pathway. We found that PLOD3, CDK1, and YAP1 were highly expressed, while LIMD1 was poorly expressed in NSCLC tissues. Mechanistic investigation demonstrated that silencing PLOD3 promoted the cleavage of PKCδ in a caspase-dependent manner to generate a catalytically active fragment cleaved PKCδ, enhanced phosphorylation levels of CDK1, and LIMD1 but suppressed nuclear translocation of YAP1. Furthermore, functional experimental results suggested that loss of PLOD3 led to increased phosphorylation levels of CDK1 and LIMD1 and downregulated YAP1, thereby suppressing the proliferation, colony formation, cell cycle entry, and resistance to apoptosis of NSCLC cells in vitro and inhibiting tumor growth in vivo. Taken together, these results show that PLOD3 silencing activates the PKCδ/CDK1/LIMD1 signaling pathway to prevent the progression of NSCLC, thus providing novel insight into molecular targets for treating NSCLC.
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