ArticleThe pharmacogenomics journal2024
The ZNF263/CPT1B axis regulates fatty acid β-oxidation to affect cisplatin resistance in lung adenocarcinoma.
Article in The pharmacogenomics journal, 2024. 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.
- Lipid Metabolic Reprogramming in Lung Cancer: Mechanisms and Therapeutic Targets in the Tumor Microenvironment.International journal of cancer · 2026Review
- Accurate, scalable and cross-platform cell identification for high-resolution spatial transcriptomics.Nature genetics · 2026Article
- Building a credibility-based framework for target discovery: Perspectives from tRNA synthetase-linked metabolic diseases.Briefings in bioinformatics · 2026Article
- (-)-Guaiol Downregulates M2 Tumor-Associated Macrophage Polarization Through PPAR-γ Signaling to Suppress Lung Cancer.Biological procedures online · 2025Article
- Integrative analysis of fatty acid metabolism and identification ofJournal of thoracic disease · 2025Article
- Metabolic reprogramming and therapeutic targeting in non-small cell lung cancer: emerging insights beyond the Warburg effect.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
Cisplatin is widely used as a conventional chemotherapy drug for lung adenocarcinoma (LUAD) patients. However, the chemical resistance greatly limits its therapeutic potential. The study aimed to uncover the specific role and new mechanisms of CPT1B in the cisplatin resistance of LUAD. Bioinformatics analysis was utilized to analyze the expression level and enriched pathway of CPT1B in LUAD. The expression of CPT1B in LUAD cells was determined by utilizing quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot (WB). The cisplatin resistance in LUAD was measured with IC
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