ArticleThe Journal of experimental medicine2021
SPRED1 deletion confers resistance to MAPK inhibition in melanoma.
Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Downregulation of SPRED1 drives keratinocyte hyperproliferation in psoriasis via activation of the ERK-RSK1 signaling axis.iScience · 2026Article
- Tumor-derived miR-126 promotes tumor progression through immune modulation beyond the local tumor environment.Frontiers in oncology · 2026Article
- The role of SPRED1 mutation in melanoma.European journal of medical research · 2025Review
- Enhancing the sensitivity of lung adenocarcinoma to immune therapeutic agents throughTranslational lung cancer research · 2025Article
- Article
- Dissecting the MAPK signaling landscape in malignant melanoma: from BRAF and NRAS mutations to precision combination therapies.Frontiers in cell and developmental biology · 2025Review
- A novel patient-derived cutaneous melanoma cell line reveals key features of metastatic melanoma.Frontiers in oncology · 2025Article
- Pigment epithelium derived factor drives melanocyte proliferation and migration in neurofibromatosis café au lait macules.Skin health and disease · 2024Article
- Prediction of CAF-related genes in immunotherapy and drug sensitivity in hepatocellular carcinoma: a multi-database analysis.Genes and immunity · 2024Article
- Long noncoding RNA LOC646029 functions as a ceRNA to suppress ovarian cancer progression through the miR-627-3p/SPRED1 axis.Frontiers of medicine · 2023Article
- Circ_TEX2 Functions as a Tumor Suppressor in Hepatoma via miR-96-5p/SPRED1 Axis.Molecular biotechnology · 2023Article
- miR-126-5p affects the chemosensitivity of colorectal cancer cells by regulatingGenes & diseases · 2023Article
- Role of dual specificity phosphatases (DUSPs) in melanoma cellular plasticity and drug resistance.Scientific reports · 2022Article
- M-CSFR/CSF1R signaling regulates myeloid fates in zebrafish via distinct action of its receptors and ligands.Blood advances · 2022Article
- RAS pathway regulation in melanoma.Disease models & mechanisms · 2022Review
- Bioluminescent Zebrafish Transplantation Model for Drug Discovery.Frontiers in pharmacology · 2022Article
- Review
- Vulvar and Vaginal Melanomas-The Darker Shades of Gynecological Cancers.Biomedicines · 2021Review
- Individualized Treatment Strategy for Cutaneous Melanoma: Where Are We Now and Where Are We Going?Frontiers in oncology · 2021Review
- SOCS, SPRED, and NR4a: Negative regulators of cytokine signaling and transcription in immune tolerance.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Functional evaluation of genetic lesions can discover a role in cancer initiation and progression and help develop novel therapeutic strategies. We previously identified the negative MAPK regulator SPRED1 as a novel tumor suppressor in KIT-driven melanoma. Here, we show that SPRED1 is also frequently deleted in human melanoma driven by mutant BRAF. We found that SPRED1 inactivation in human melanoma cell lines and primary zebrafish melanoma conferred resistance to BRAFV600E inhibition in vitro and in vivo. Mechanistically, SPRED1 loss promoted melanoma cell proliferation under mutant BRAF inhibition by reactivating MAPK activity. Consistently, biallelic deletion of SPRED1 was observed in a patient whose melanoma acquired resistance to MAPK-targeted therapy. These studies combining work in human cells and in vivo modeling in zebrafish demonstrate a new mechanism of resistance to BRAFV600E inhibition in melanoma.
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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.