ArticleOncotarget2016
Overcoming melanoma resistance to vemurafenib by targeting CCL2-induced miR-34a, miR-100 and miR-125b.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 65 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
65 citing papers in PubMed, 104 citations in OpenAlex.
- Genomic, Clinical, and Spatial Predictors of Durable Response to BRAF/MEK Inhibition inbioRxiv : the preprint server for biology · 2026Article
- SPACA6-hosted miR-99b~125a~let-7e cluster shapes melanoma resistance by modulating mTOR-mediated immunosuppression.Frontiers in immunology · 2025Article
- Non-coding RNAs in BRAF-mutant melanoma: targets, indicators, and therapeutic potential.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Advances in Understanding Drug Resistance Mechanisms and Innovative Clinical Treatments for Melanoma.Current treatment options in oncology · 2024Review
- Cold and hot tumors: from molecular mechanisms to targeted therapy.Signal transduction and targeted therapy · 2024Review
- Characterization of two melanoma cell lines resistant to BRAF/MEK inhibitors (vemurafenib and cobimetinib).Cell communication and signaling : CCS · 2024Article
- Circulating interleukin-8 and osteopontin are promising biomarkers of clinical outcomes in advanced melanoma patients treated with targeted therapy.Journal of experimental & clinical cancer research : CR · 2024Article
- Exploring resistance to immune checkpoint inhibitors and targeted therapies in melanoma.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Proliferating macrophages in human tumours show characteristics of monocytes responding to myelopoietic growth factors.Frontiers in immunology · 2024Article
- Article
- Pathology and Molecular Biology of Melanoma.Current issues in molecular biology · 2023Review
- Comparative Expression Profiling Reveals Molecular Markers Involved in the Progression of Cutaneous Melanoma towards Metastasis.International journal of molecular sciences · 2023Article
- MicroRNA as a Diagnostic Tool, Therapeutic Target and Potential Biomarker in Cutaneous Malignant Melanoma Detection-Narrative Review.International journal of molecular sciences · 2023Review
- Kisspeptin-mediated improvement of sensitivity to BRAF inhibitors in vemurafenib-resistant melanoma cells.Frontiers in oncology · 2023Article
- Role of miRNA in Melanoma Development and Progression.International journal of molecular sciences · 2022Review
- Epigenetic Mechanisms Underlying Melanoma Resistance to Immune and Targeted Therapies.Cancers · 2022Review
- BRAF Inhibitor Resistance in Melanoma: Mechanisms and Alternative Therapeutic Strategies.Current treatment options in oncology · 2022Review
- Current understanding of epigenetics role in melanoma treatment and resistance.Cancer cell international · 2022Review
- Review
- Visual barcodes for clonal-multiplexing of live microscopy-based assays.Nature communications · 2022Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
21 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In melanoma, the adaptative cell response to BRAF inhibitors includes altered patterns of cytokine production contributing to tumor progression and drug resistance. Among the factors produced by PLX4032-resistant melanoma cell lines, CCL2 was higher compared to the sensitive parental cell lines and increased upon drug treatment. CCL2 acted as an autocrine growth factor for melanoma cells, stimulating the proliferation and resistance to apoptosis. In patients, CCL2 is detected in melanoma cells in tumors and in plasma at levels that correlate with tumor burden and lactate dehydrogenase. Vemurafenib treatment increased the CCL2 levels in plasma, whereas the long-term clinical response was associated with low CCL2 levels.Increased CCL2 production was associated with miRNA deregulation in the resistant cells. miR-34a, miR-100 and miR-125b showed high expression in both resistant cells and in tumor biopsies that were obtained from treated patients, and they were involved in the control of cell proliferation and apoptosis. Inhibition of CCL2 and of the selected miRNAs restored both the cell apoptosis and the drug efficacy in resistant melanoma cells. Therefore, CCL2 and miRNAs are potential prognostic factors and attractive targets for counteracting treatment resistance in metastatic melanoma.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.