ArticleGenes & genomics2019
Upregulation of S100A9 contributes to the acquired resistance to BRAF inhibitors.
Article in Genes & genomics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- S100A8-associated inflammatory microenvironment is related to its cell-of-origin and potentiates BRAF inhibitor resistance in papillary craniopharyngioma.Clinical and experimental medicine · 2026Article
- SOX10, MITF, and microRNAs: Decoding their interplay in regulating melanoma plasticity.International journal of cancer · 2025Review
- Comparative analysis of clinical features, methylation and immune microenvironment in pediatric and adult papillary craniopharyngiomas: results from a multicenter study.Scientific reports · 2025Article
- Metastatic Melanoma Treatment and Prophylaxis with S100A9-Targeting Cowpea Mosaic Virus Nanoparticles.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Alarmins in cutaneous malignant melanoma: An updated overview of emerging evidence on their pathogenetic, diagnostic, prognostic, and therapeutic role.The Journal of dermatology · 2024Review
- Blocking S100A9-signaling is detrimental to the initiation of anti-tumor immunity.Frontiers in immunology · 2024Article
- Metastatic Colon Cancer Treatment Using S100A9-Targeted Cowpea Mosaic Virus Nanoparticles.Biomacromolecules · 2022Article
- RNA-seq and ChIP-seq Identification of Unique and Overlapping Targets of GLI Transcription Factors in Melanoma Cell Lines.Cancers · 2022Article
- Review
- Hypoxia-Induced Adaptations of miRNomes and Proteomes in Melanoma Cells and Their Secreted Extracellular Vesicles.Cancers · 2020Article
- Cancer stem cells, plasticity, and drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2020Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundsAcquired resistance is a significant clinical challenge in targeted therapy of melanomas using BRAF inhibitors. We previously identified that downregulation of miR-92a-1-5p confers acquired resistance to BRAF inhibition using an miRNA array platform.
objectiveIn this study, we investigated the target genes of miR-92a-1-5p and their functional significance in BRAF inhibitor resistance.
methodsThe miRNA target prediction data were combined with RNA-Seq data to identify possible target genes for miR-92a-1-5p. Cellular effects of target genes were further examined using siRNA knockdown, WST-1 assay, and immunoblotting analysis.
resultsWe selected S100 calcium-binding protein A9 (S100A9) as a possible target gene for functional validation. S100A9 knockdown abrogated resistance to PLX4720 in A375P/Mdr cells. This result was similar to those described earlier for miR-92a-1-5p, indicating that miR-92a-1-5p inhibits cell viability by targeting S100A9. S100A9 overexpression partially conferred PLX4720 resistance to A375P cells. We also demonstrated that MAPK re-activation does not contribute to the promotion of BRAF inhibitor resistance by S100A9.
conclusionTaken together, our results indicate that S100A9 might be functionally involved in development of resistance to BRAF inhibitors and might be a target for melanoma therapy in the future.
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