ArticleHeliyon2024
Transcriptome analysis reveals PRKCA as a potential therapeutic target for overcoming cisplatin resistance in lung cancer through ferroptosis.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- [Overexpression of miR-183-5p enhances malignant phenotype and inhibits ferroptosis of triple-negative breast cancer cells by negatively regulating KLHL24].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Integrative phosphoproteomic network analysis identifies CAMK2D as a shared regulator of TPD52 family proteins in cancer.Protoplasma · 2026Article
- Article
- Identification and validation of biomarkers of Shenggu Zaizao Wan in the treatment of steroid-induced osteonecrosis of the femoral head by integrating network pharmacology and bulk transcriptomic.Frontiers in medicine · 2026Article
- Decoding the molecular mechanism via systems biology-based insights into neoschaftoside from Ailanthus altissima targeting lung cancer.Scientific reports · 2025Article
- MOF promotes cisplatin resistance in lung cancer cells by enhancing WSTF acetylation.In vitro cellular & developmental biology. Animal · 2025Article
- CircPRKCA facilitates esophageal squamous cell carcinoma metastasis via m5C-dependent CSF2 mRNA stabilization.Journal of translational medicine · 2025Article
- Dual-specificity phosphatase 23 functions as a promising prognostic biomarker in non-small cell lung cancer.Genes & genomics · 2025Article
- An early-stage 3D fibroblast-featured tumor model mimics the gene expression of the naïve tumor microenvironment, including genes involved in cancer progression and drug resistance.Frontiers in oncology · 2025Article
- Identification of potential immune-related genes and infiltrations in temporomandibular joint osteoarthritis.Annals of medicine and surgery (2012) · 2024Article
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Authors and funding
11 authors.
Funding
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Abstract
Cisplatin-based chemotherapy is the current standard care for lung cancer patients; however, drug resistance frequently develops during treatment, thereby limiting therapeutic efficacy.The molecular mechanisms underlying cisplatin resistance remain elusive. In this study, we conducted an analysis of microarray data from the Gene Expression Omnibus (GEO) database under the accession numbers GSE21656, which encompassed expression profiling of cisplatin-resistant H460 (DDP-H460)and the parental cells (H460). Subsequently, we calculated the differentially expressed genes (DEGs) between DDP-H460 and H460. Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of DEGs demonstrated significant impact on the Rap1, PI3K/AKT and MAPK signaling pathways. Moreover, protein and protein interaction (PPI) network analysis identified PRKCA, DET1, and UBE2N as hub genes that potentially contribute predominantly to cisplatin resistance. Ultimately, PRKCA was selected for validation due to its significant prognostic effect, which predicts unfavorable overall survival and disease-free survival in patients with lung cancer. Network analysis conducted on The Cancer Genome Atlas (TCGA) database revealed a strong gene-level correlation between PRKCA and TP53, CDKN2A, BYR2, TTN, KRAS, and PIK3CA; whereas at the protein level, it exhibited a high correlation with EGFR, Lck, Bcl2, and Syk. The in vitro experiments revealed that
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