miR-146a-5p impairs melanoma resistance to kinase inhibitors by targeting COX2 and regulating NFkB-mediated inflammatory mediators
Open accessAbstract
Background: Targeted therapy with BRAF and MEK inhibitors has improved the survival of patients with BRAF-mutated metastatic melanoma, but most patients relapse upon the onset of drug resistance induced by mechanisms including genetic and epigenetic events. Among the epigenetic alterations, microRNA perturbation is associated with the development of kinase inhibitor resistance. Here, we identified and studied the role of miR-146a-5p dysregulation in melanoma drug resistance. Methods: The miR-146a-5p-regulated NFkB signaling network was identified in drug-resistant cell lines and melanoma tumor samples by expression profiling and knock-in and knock-out studies. A bioinformatic data analysis identified COX2 as a central gene regulated by miR-146a-5p and NFkB. The effects of miR-146a-5p/COX2 manipulation were studied in vitro in cell lines and with 3D cultures of treatment-resistant tumor explants from patients progressing during therapy. Results: miR-146a-5p expression was inversely correlated with drug sensitivity and COX2 expression and was reduced in BRAF and MEK inhibitor-resistant melanoma cells and tissues. Forced miR-146a-5p expression reduced COX2 activity and significantly increased drug sensitivity by hampering prosurvival NFkB signaling, leading to reduced proliferation and enhanced apoptosis. Similar effects were obtained by inhibiting COX2 by celecoxib, a clinically approved COX2 inhibitor. Conclusions: Deregulation of the miR-146a-5p/COX2 axis occurs in the development of melanoma resistance to targeted drugs in melanoma patients. This finding reveals novel targets for more effective combination treatment. Graphical Abstract:
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Celecoxib enhances the efficacy of BRAF/MEKi treatments in melanoma through suppression of the NF-κB pathway.
“Celecoxib has been shown to enhance the efficacy of BRAF/MEKi treatments in melanoma through suppression of the NF-κB pathway.”
From Drug repurposing for cancer therapy (2024) · cites this paper as [183]
The Results section (“Targeting COX2 restores melanoma sensitivity to BRAF/MEKi”; page unavailable) supports increased growth inhibition and cytotoxicity with celecoxib plus BRAF/MEKi in melanoma cells. But it reports noncanonical NF-κB activation, not suppression, and attributes the enhanced apoptotic effects to reduced PGE2 production. The Discussion likewise describes activation of NF-κB signaling cascades during celecoxib-induced cell death. (LLM, conf=0.88)
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Experimental — accuracy not yet measuredCOX-2 promotes resistance of melanoma cells to kinase inhibitors through regulation of NF-κB-mediated inflammatory mediators.
“COX-2 promotes the resistance of melanoma cells to kinase inhibitors through the regulation of NF-κB -mediated inflammatory mediators”
From Drug repurposing for cancer therapy (2024) · cites this paper as [183]
The Results section (‘Targeting COX2 restores melanoma sensitivity to BRAF/MEKi’; page not provided) reports that COX2 knockdown increased melanoma-cell sensitivity to the inhibitors. But the paper attributes the reduction of NF-κB-induced inflammatory mediators to miR-146a expression; it explains the effect of COX2 inhibition on drug sensitivity through reduced PGE2 production, not through COX2 regulation of those mediators. (LLM, conf=0.86)
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Sex-divergent neurovascular and cognitive effects of chronic cerebral hypoperfusion
Kirby, B. D., Clary, B. L., Burrage, E. N., Chantler, P. D., Dakhlallah, D. A., Karelina, K., Brown, C. M., & Simpkins, J. W. (2026) · Experimental Neurology · doi:10.1016/j.expneurol.2026.116066
- Authors
- Vergani, E., Dugo, M., Cossa, M., Frigerio, S., Di Guardo, L., Gallino, G., Mattavelli, I., Vergani, B., Lalli, L., Tamborini, E., Valeri, B., Gargiuli, C., Shahaj, E., Ferrarini, M., Ferrero, E., Gomez Lira, M., Huber, V., Del Vecchio, M., Sensi, M., Leone, B. E., Santinami, M., Rivoltini, L., Rodolfo, M., & Vallacchi, V.
- Affiliations
- Fondazione IRCCS Istituto Nazionale dei Tumori (IT)
- University of Milano-Bicocca (IT)
- IRCCS Ospedale San Raffaele (IT)
- Corresponding author
- Vallacchi, Viviana
- ORCID
- Vergani, Elisabetta
- Dugo, Matteo
- Cossa, Mara
- Frigerio, Simona
- Gallino, Gianfrancesco
- Mattavelli, Ilaria
- Vergani, Barbara
- Lalli, Luca
- Tamborini, Elena
- Valeri, Barbara
- Gargiuli, Chiara
- Shahaj, Eriomina
- Ferrarini, Marina
- Ferrero, Elisabetta
- Huber, Veronica
- Sensi, Marialuisa
- Leone, Biagio Eugenio
- Santinami, Mario
- Rivoltini, Licia
- Rodolfo, Monica
- Vallacchi, Viviana
- Venue
- Cell Communication and Signaling
- Published
- 2020-09-23
- Volume
- 18
- Issue
- 1
- Pages
- 156-156
- ISSN
- 1478-811X (ISSN-L)
- PMC
- PMC7510138
- OpenAlex
- W3088238859
- Cited by
- 39
- References
- 49
- Citations by year
- 2026: 9 · 2025: 6 · 2024: 5 · 2023: 8 · 2022: 9 · 2021: 2
- FWCI
- 1.54
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cell Communication and Signaling (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- BOA (University of Milano-Bicocca) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Fondazione Cariplo (2015-0911)
- Associazione Italiana per la Ricerca sul Cancro (IG 17462, 5x1000 no. 12162)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Keywords
- miR-146a, melanoma, kinase inhibitor resistance, BRAF inhibitors, MEK inhibitors, cyclooxygenase-2, NF-κB signaling, microRNA, celecoxib, epigenetic drug resistance, inflammatory mediators, apoptosis, combination therapy
- MeSH terms
- Humans, Melanoma, Models, Biological, Signal Transduction, Gene Expression Regulation, Neoplastic, NF-kappa B, Inflammation Mediators, Drug Resistance, Neoplasm, Mitogen-Activated Protein Kinase Kinases, MicroRNAs, Cell Line, Tumor, Protein Kinase Inhibitors, Extracellular Signal-Regulated MAP Kinases, Proto-Oncogene Proteins B-raf, Proto-Oncogene Proteins c-akt, Cyclooxygenase 2
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