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Dabrafenib resistance is a significant problem in melanoma, and its underlying molecular mechanism is still unclear. The purpose of this study is to research the molecular mechanism of drug resistance of dabrafenib and to explore the key genes and pathways that mediate drug resistance in melanoma. GSE117666 was downloaded from the Gene Expression Omnibus (GEO) database and 492 melanoma statistics were also downloaded from The Cancer Genome Atlas (TCGA) database. Besides, differentially expressed miRNAs (DEMs) were identified by taking advantage of the R software and GEO2R. The Database for Annotation, Visualization, and Integrated Discovery (DAVID) and FunRich was used to perform Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis to identify potential pathways and functional annotations linked with melanoma chemoresistance. 9 DEMs and 872 mRNAs were selected after filtering. Then, target genes were uploaded to Metascape to construct protein-protein interaction (PPI) network. Also, 6 hub mRNAs were screened after performing the PPI network. Furthermore, a total of 4 out of 9 miRNAs had an obvious association with the survival rate ( < 0.05) and showed a good power of risk prediction model of over survival. The present research may provide a deeper understanding of regulatory genes of dabrafenib resistance in melanoma.
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http://dx.doi.org/10.1155/2021/5524486 | DOI Listing |
Dermatol Reports
August 2025
Department of Oral and Maxillofacial Head and Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine.
Improving insights into the current research and literature on melanoma is useful for healthcare providers to apply the latest advancements for offering better care to patients. Herein, this bibliometric study analyzed the characteristics and trends in melanoma research through the top-cited articles. The top 100 most cited articles on melanoma were published between 1969 and 2020, and the average number of citations was 36.
View Article and Find Full Text PDFInt J Biol Macromol
September 2025
State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xi'an, Shaanxi 710032, PR China. Electronic address:
Glioma, a primary intracranial malignancy with high morbidity and mortality, remains therapeutically challenging despite of advances in targeted and immune therapies. ZCCHC9, a ZCCHC family member predominantly expressed in brain cortex, has documented roles in cervical and non-small cell lung cancer, yet its function, mechanism, and clinical significance in glioma is unclear. Through multi-omics analyses leveraging TCGA, CGGA, and HPA platforms, we identified aberrant up-regulation of ZCCHC9 in glioma, particularly in grade IV, older patients, and adverse molecular subtypes, e.
View Article and Find Full Text PDFInt J Mol Sci
July 2025
Department of Physiology and Biochemistry, Faculty of Medicine and Surgery, University of Malta, MSD 2080 Msida, Malta.
Malignant cutaneous melanoma is among the most aggressive forms of skin cancer, characterized by high metastatic potential and frequent resistance to standard therapies. Hydroxytyrosol, a phenolic compound derived from extra virgin olive oil, has shown promising anticancer properties in various models, yet its effects in 3D melanoma systems remain poorly understood. In this study, we used paired 3D spheroid models of non-tumorigenic (HEMa) and melanoma (C32) to assess the therapeutic potential of hydroxytyrosol.
View Article and Find Full Text PDFbioRxiv
June 2025
Surgical Oncology Program, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892.
Anaplastic thyroid cancer (ATC) is the most aggressive form of thyroid cancer. Despite recent advances in treating BRAFV600E-driven ATC, therapy resistance remains a significant challenge, often resulting in disease progression and death. Leveraging a focused CRISPR/KO screen in parallel with a CRISPR/activation screen, both tailored on response to BRAFV600E inhibitor treatment, we identified TAZ (encoded by the WWTR1 gene) deficiency as synthetically lethal with BRAF inhibitor in ATC.
View Article and Find Full Text PDFPurpose: While combination BRAF and MEK inhibitor treatment in -mutant cancers results in a response, treatment resistance and toxicity are common. Ferroptosis is an iron-dependent form of non-apoptotic cell death. BRAF inhibition has been associated with increased sensitivity to ferroptosis that is dependent on Glutathione Peroxidase 4 (GPX4).
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