ArticleScientific reports2024
PDGFBB facilitates tumorigenesis and malignancy of lung adenocarcinoma associated with PI3K-AKT/MAPK signaling.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Novel Blood-Based Extracellular Vesicle-Derived Biomarkers in Small Cell Lung Cancer Identified via Proximity Extension Assay.Cancers · 2026Article
- Stabilization of RUNX1 Induced by O-GlcNAcylation Promotes PDGF-BB-Mediated Resistance to CDK4/6 Inhibitors in Breast Cancer.Cancer research · 2025Article
- The CoREST complex is a therapeutic vulnerability in malignant peripheral nerve sheath tumors.Scientific reports · 2025Article
- m6A-Mediated Stabilization of PRMT9 mRNA by IGF2BP1 Drives Proliferation and Metastasis in Lung Adenocarcinoma.Analytical cellular pathology (Amsterdam) · 2025Article
- Identification of locally advanced rectal cancer-related genes based on transcriptome and mendelian randomization analysis with biological validation.Frontiers in immunology · 2025Article
- Article
- Diagnostic and prognostic value of coagulation markers and platelet-derived growth factor-BB in evaluating intensity-modulated radiotherapy efficacy in nasopharyngeal carcinoma.American journal of cancer research · 2025Article
- Artemisinin derivatives maintain fibroblast normalization by acting on tumor-stroma interactions in oral tongue squamous cell carcinoma.American journal of cancer research · 2025Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Lung adenocarcinoma (LUAD) remains one of the most aggressive tumors and the efficacy of conventional treatment has been bleak. Nowadays, gene-targeted therapy has become a new favorite in tumor therapy. Herein, we investigated the effect of platelet derived growth factor BB (PDGFBB) on LUAD. Firstly, PDGFBB was upregulated in LUAD patients and closely linked with poor survival. Furthermore, the expression of PDGFBB and PDGFRα/β in LUAD cells was higher than that in normal lung cells. By loss-of-function with herpes simplex virus (HSV)-PDGFi-shRNA, we found that PDGFBB knockdown caused a significant decrease in proliferation and migration, but evoked apoptosis of LUAD cells in vitro. Conversely, exogenous PDGFBB held adverse effect. Additionally, A549 cells with PDGFBB knockdown had a low probability of tumorigenesis in vivo. Moreover, PDGFBB knockdown restrained the growth of xenografts derived from normal A549 cells. Mechanistically, PDGFBB knockdown suppressed PI3K/AKT and Ras/MAPK signaling, while PDGFBB was the opposite. Therefore, we concluded that PDGFBB might facilitate the tumorigenesis and malignancy of LUAD through its functional downstream nodes-PI3K/AKT and Ras/MAPK signaling, which supported that PDGFBB could serve as a rational therapeutic target for LUAD.
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