ArticleBiomolecules & therapeutics2019
Differential Gene Expression Common to Acquired and Intrinsic Resistance to BRAF Inhibitor Revealed by RNA-Seq Analysis.
Article in Biomolecules & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- C-Terminal Hsp90 Inhibitors Overcome MEK and BRAF Inhibitor Resistance in Melanoma.Journal of cellular and molecular medicine · 2025Article
- SEMA6A/RhoA/YAP axis mediates tumor-stroma interactions and prevents response to dual BRAF/MEK inhibition in BRAF-mutant melanoma.Journal of experimental & clinical cancer research : CR · 2022Article
- Article
- Transcriptomics Changes in the Peritoneum of Mice with Lipopolysaccharide-Induced Peritonitis.International journal of molecular sciences · 2021Article
- PTENP1-AS contributes to BRAF inhibitor resistance and is associated with adverse clinical outcome in stage III melanoma.Scientific reports · 2021Article
- Transcriptomic Changes in Mouse Bone Marrow-Derived Macrophages Exposed to Neuropeptide FF.Genes · 2021Article
- Prolactin-Releasing Peptide Differentially Regulates Gene Transcriptomic Profiles in Mouse Bone Marrow-Derived Macrophages.International journal of molecular sciences · 2021Article
- Pan-Cancer Transcriptional Models Predicting Chemosensitivity in Human Tumors.Cancer informatics · 2021Article
- Therapeutic Effects of Specialized Pro-Resolving Lipids Mediators on Cardiac Fibrosis via NRF2 Activation.Antioxidants (Basel, Switzerland) · 2020Review
- Gene Expression Signature of BRAF Inhibitor Resistant Melanoma Spheroids.Pathology oncology research : POR · 2020Article
- Review
- Hub Proteins Involved in RAW 264.7 Macrophages Exposed to Direct Current Electric Field.International journal of molecular sciences · 2020Article
- Functional and transcriptomic characterization of cisplatin-resistant AGS and MKN-28 gastric cancer cell lines.PloS one · 2020Article
- Cellular Processes Involved in Jurkat Cells Exposed to Nanosecond Pulsed Electric Field.International journal of molecular sciences · 2019Article
- Upregulation of S100A9 contributes to the acquired resistance to BRAF inhibitors.Genes & genomics · 2019Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Melanoma cells have been shown to respond to BRAF inhibitors; however, intrinsic and acquired resistance limits their clinical application. In this study, we performed RNA-Seq analysis with BRAF inhibitor-sensitive (A375P) and -resistant (A375P/Mdr with acquired resistance and SK-MEL-2 with intrinsic resistance) melanoma cell lines, to reveal the genes and pathways potentially involved in intrinsic and acquired resistance to BRAF inhibitors. A total of 546 differentially expressed genes (DEGs), including 239 up-regulated and 307 down-regulated genes, were identified in both intrinsic and acquired resistant cells. Gene ontology (GO) analysis revealed that the top 10 biological processes associated with these genes included angiogenesis, immune response, cell adhesion, antigen processing and presentation, extracellular matrix organization, osteoblast differentiation, collagen catabolic process, viral entry into host cell, cell migration, and positive regulation of protein kinase B signaling. In addition, using the PANTHER GO classification system, we showed that the highest enriched GOs targeted by the 546 DEGs were responses to cellular processes (ontology: biological process), binding (ontology: molecular function), and cell subcellular localization (ontology: cellular component). Ingenuity pathway analysis (IPA) network analysis showed a network that was common to two BRAF inhibitor-resistant cells. Taken together, the present study may provide a useful platform to further reveal biological processes associated with BRAF inhibitor resistance, and present areas for therapeutic tool development to overcome BRAF inhibitor resistance.
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