ArticleJournal of cellular physiology2020
RANKL triggers resistance to TRAIL-induced cell death in oral squamous cell carcinoma.
Article in Journal of cellular physiology, 2020. 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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The trial behind it
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- LINC00514 regulates oral squamous cell carcinoma progression and prognosis by targeting miR-195-5p.BMC oral health · 2026Article
- INHBA: a mitochondrial-related pan-cell death gene associated with the prognosis and immunity of OSCC.Scientific reports · 2026Article
- TMEM131-Mediated Soluble TRAIL Triggered Type II Alveolar Epithelial Cell Senescence in Radiation-Induced Lung Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Increased V-ATPase activity can lead to chemo-resistance in oral squamous cell carcinoma via autophagy induction: new insights.Medical oncology (Northwood, London, England) · 2024Review
- Dual roles of cellular communication network factor 6 (CCN6) in the invasion and metastasis of oral cancer cells to bone via binding to BMP2 and RANKL.Carcinogenesis · 2023Article
- MicroRNA let-7i-3p affects osteoblast differentiation in ankylosing spondylitis via targeting PDK1.Cell cycle (Georgetown, Tex.) · 2021Article
- Harnessing TRAIL-Induced Apoptosis Pathway for Cancer Immunotherapy and Associated Challenges.Frontiers in immunology · 2021Review
- Role of Autophagy in the Microenvironment of Oral Squamous Cell Carcinoma.Frontiers in oncology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Oral squamous cell carcinoma (OSCC) occurs as a malignancy of the oral cavity. RANK ligand (RANKL) is essential for osteoclast formation/bone resorption. Recently, we showed autoregulation of receptor activator of nuclear factor-κB ligand (RANKL) stimulates OSCC cell proliferation. OSCC cells show resistance to tumor necrosis factor related apoptosis inducing ligand (TRAIL) treatment. Therefore, we hypothesize that RANKL promotes resistance for TRAIL induction of OSCC apoptotic cell death. In this study, SCC14A and SCC74A cells cultured with TRAIL revealed high-level expression of RANKL which increased resistance to TRAIL inhibition of tumor cell proliferation. RANKL stimulation inhibited terminal deoxynucleotidyl transferase dUTP nick end labeling positive staining in TRAIL-treated cells. CRISPR/Cas-9 knockout of RANKL (RANKL-KO) increased caspase-9, caspase-3 activity and cytochrome c release in OSCC cells. RANKL inhibited proapoptotic proteins BAD and BAX expression. TRAIL treatment suppressed the SQSTM1/p62 and RANKL restored the expression. Interestingly, RANKL alone significantly increased proteasome activity. RANKL-KO in OSCC cells inhibited autophagic activity as evidenced by decreased light chain 3B-II and beclin-1 expression. Thus, RANKL stimulation of OSCC tumor cells triggered resistance for TRAIL-induced OSCC cell death. Taken together, blockade of RANKL may inhibit OSCC tumor progression and enhance the potential of TRAIL induced OSCC tumor cell apoptosis.
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Registered trials
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