ArticleThoracic cancer2023
RANKL acts an unfavorable prognostic biomarker and potential target in advanced KRAS-mutated lung adenocarcinoma.
Article in Thoracic cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- RNA modifications in radiotherapy resistance and radiosensitization: epitranscriptomic regulation of tumor response to radiation.Frontiers in cell and developmental biology · 2026Review
- Duration-Dependent Lung Injury Induced by High-Intensity Electric Field Exposure: Histopathological and Immunoinflammatory Insights.International journal of molecular sciences · 2025Article
- RANKL/PD-1 dual blockade demonstrates survival benefit for patients with advanced lung adenocarcinoma harboring KRAS mutations.Cell reports. Medicine · 2025Article
- LAMA3 overexpression enhances proliferation, migration and invasion in esophageal squamous cell carcinoma based on bioinformatics and experimental validation.Scientific reports · 2025Article
- Assessing EGFR-mutated NSCLC with bone metastasis: Clinical features and optimal treatment strategy.Cancer medicine · 2024Article
- RANKL acts an unfavorable prognostic biomarker and potential target in advanced KRAS-mutated lung adenocarcinoma.Thoracic cancer · 2023Article
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3 authors at 1 institution in 1 country.
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Abstract
objectiveAdvanced lung cancers carrying Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation remain a group that lacks effective treatments. Receptor activator of nuclear factorκB ligand (RANKL) has been demonstrated to drive malignant phenotypes in lung cancer; however, its role in KRAS-mutant (mt) lung adenocarcinoma (LUAD) is not yet fully elucidated. MATERIALS AND
methodsThe data used to explore expression and prognosis were obtained from The Cancer Genome Atlas, Genotype-Tissue Expression databases, and from our hospital. The proliferation, invasion, and migration capacities of KRAS-mt LUAD cells were evaluated. The prediction model was established via Lasso regression method.
resultsRANKL is strongly expressed in advanced KRAS-mt LUAD, and significantly distinct association exists between high RANKL expression and poor survival. The enriched expression of RANKL in advanced KRAS-mt LUAD was confirmed by specimens from our hospital. Further, although not statistically significant, our clinical cohort (n = 57) revealed a longer median progression-free survival in advanced KRAS-mt LUAD patients treated with RANKL inhibitor than those without (300 vs. 133 days, p = 0.210), but not in KRAS-wt ones (208 vs. 250 days, p = 0.334). Decrease of KRAS-mt LUAD cells' capacity for proliferation, invasion, and migration was observed when RANKL was knocked down. Enrichment analysis suggested distinct roles of RANKL between KRAS-mt and KRAS-wt LUAD, with adhesion-related pathways and molecules significantly downregulated in the KRAS-mt RANKL-high tumors. Finally, a model for predicting overall survival of KRAS-wt LUAD was established according to four related key genes (BCAM, ICAM5, ITGA3, and LAMA3), which had good performance in prediction concordance.
conclusionsRANKL acts as an unfavorable prognostic biomarker for patients with advanced KRAS-mt LUAD. Inhibition of RANKL may be a feasible strategy for this subset of patients.
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