ArticleOncogene2017
Inhibition of the CRAF/prohibitin interaction reverses CRAF-dependent resistance to vemurafenib.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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Who cites it
25 citing papers in PubMed, 35 citations in OpenAlex.
- Integrative multi-omics defines melanoma drug response networks and ARID1A-dependent resistance mechanisms.Molecular systems biology · 2026Article
- Research Progress of Natural Compounds from Chinese Herbal Medicine in the Treatment of Melanoma.Current treatment options in oncology · 2025Review
- The evolution of BRAF-targeted therapies in melanoma: overcoming hurdles and unleashing novel strategies.Frontiers in oncology · 2024Review
- Targeting CRAF kinase in anti-cancer therapy: progress and opportunities.Molecular cancer · 2023Review
- Review
- Targeting RAS-RAF-MEK-ERK signaling pathway in human cancer: Current status in clinical trials.Genes & diseases · 2023Review
- Analyses of Transcriptomics Cell Signalling for Pre-Screening Applications in the Integrated Approach for Testing and Assessment of Non-Genotoxic Carcinogens.International journal of molecular sciences · 2022Review
- Genomic and Transcriptomic Underpinnings of Melanoma Genesis, Progression, and Metastasis.Cancers · 2021Review
- Targeted intervention of eIF4A1 inhibits EMT and metastasis of pancreatic cancer cells via c-MYC/miR-9 signaling.Cancer cell international · 2021Article
- Simultaneous blocking of the pan-RAF and S100B pathways as a synergistic therapeutic strategy against malignant melanoma.Journal of cellular and molecular medicine · 2021Article
- Role of Prohibitins in Aging and Therapeutic Potential Against Age-Related Diseases.Frontiers in genetics · 2021Review
- Mechanisms of Resistance to BRAF-Targeted Melanoma Therapies.American journal of clinical dermatology · 2021Article
- A20 regulates the therapeutic effect of anti-PD-1 immunotherapy in melanoma.Journal for immunotherapy of cancer · 2020Article
- Review
- Prohibitin ligands: a growing armamentarium to tackle cancers, osteoporosis, inflammatory, cardiac and neurological diseases.Cellular and molecular life sciences : CMLS · 2020Review
- A novel function of Prohibitin on melanosome transport in melanocytes.Theranostics · 2020Article
- BRAF in malignant melanoma progression and metastasis: potentials and challenges.American journal of cancer research · 2020Review
- Cancer stem cells, plasticity, and drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2020Review
- Prohibitin promotes de-differentiation and is a potential therapeutic target in neuroblastoma.JCI insight · 2019Article
- Significance of prohibitin domain family in tumorigenesis and its implication in cancer diagnosis and treatment.Cell death & disease · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Activating BRAF mutations promote constitutive activation of the mitogen-activated protein kinase (MAPK) signaling pathway and are common in a variety of human malignancies, including melanoma and colon cancer. Several small molecule BRAF inhibitors such as vemurafenib have been developed and demonstrate remarkable clinical efficacy. However, resistance typically emerges in most melanoma patients. Studies have demonstrated that reactivation of MAPK signaling via CRAF overexpression and dysregulation is a mechanism for vemurafenib resistance in melanoma. Prohibitins (PHBs) are highly conserved proteins that are thought to control the cell cycle, senescence and tumor suppression. PHB1 is essential for CRAF-mediated ERK1/2 activation through direct binding to CRAF. We developed a CRAF-mediated model of vemurafenib resistance in melanoma cells to assess the importance of the interaction between CRAF and PHB1 in resistance to BRAF-targeting agents. We demonstrate that CRAF overexpression renders melanoma cells resistant to BRAF-targeting agents. Moreover, treatment with the natural compound rocaglamide A disrupts the interaction between PHB and CRAF in melanoma cells, thus reducing MEK1/2 and ERK1/2 signaling, inhibiting melanoma cell growth and inducing apoptosis. The efficacy of these compounds was also demonstrated in a human melanoma xenograft model. Taken together, these data suggest that PHB1 may serve as a novel, druggable target in CRAF-mediated vemurafenib resistance.
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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.