ArticleCancer research2015
SBI-0640756 Attenuates the Growth of Clinically Unresponsive Melanomas by Disrupting the eIF4F Translation Initiation Complex.
Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- Targeting the eIF4F translation initiation complex disrupts BCR::ABL1 translation and overcomes drug resistance in CML.Leukemia · 2026Article
- Translational control of AMPK activity in melanoma.Cell communication and signaling : CCS · 2026Article
- E0703 targets ERβ to facilitate the upregulation of GLI3, thereby alleviating irradiation-induced DNA damage on lymphocytes.Cellular & molecular biology letters · 2025Article
- Guidelines for minimal reporting requirements, design and interpretation of experiments involving the use of eukaryotic dual gene expression reporters (MINDR).Nature structural & molecular biology · 2025Review
- Link between Parkinson's disease and melanoma: insights into the influence of theFrontiers in oncology · 2025Review
- eIF4F controls ERK MAPK signaling in melanomas withProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Reprograming immunosuppressive microenvironment by eIF4G1 targeting to eradicate pancreatic ductal adenocarcinoma.Cell reports. Medicine · 2024Article
- N-MYC regulates cell survival via eIF4G1 in inv(16) acute myeloid leukemia.Science advances · 2024Article
- The role of eIF4F-driven mRNA translation in regulating the tumour microenvironment.Nature reviews. Cancer · 2023Review
- Article
- Adaptive translational reprogramming of metabolism limits the response to targeted therapy in BRAFNature communications · 2022Article
- Inhibition of coronavirus HCoV-OC43 by targeting the eIF4F complex.Frontiers in pharmacology · 2022Article
- Metabolic Plasticity in Melanoma Progression and Response to Oncogene Targeted Therapies.Cancers · 2021Review
- Targeting eIF4F translation complex sensitizes B-ALL cells to tyrosine kinase inhibition.Scientific reports · 2021Article
- Identification of Novel Therapeutic Targets for Fibrolamellar Carcinoma Using Patient-Derived Xenografts and Direct-from-Patient Screening.Cancer discovery · 2021Article
- Reduced eIF4E function impairs B-cell leukemia without altering normal B-lymphocyte function.iScience · 2021Article
- A decision process for drug discovery in retinoblastoma.Investigational new drugs · 2021Article
- Elevation of EIF4G1 promotes non-small cell lung cancer progression by activating mTOR signalling.Journal of cellular and molecular medicine · 2021Article
- Role of EIF4G1 network in non-small cell lung cancers (NSCLC) cell survival and disease progression.Journal of cellular and molecular medicine · 2021Article
- Targeting eIF4F translation initiation complex with SBI-756 sensitises B lymphoma cells to venetoclax.British journal of cancer · 2021Article
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 2 countries.
Funding
Abstract
Disrupting the eukaryotic translation initiation factor 4F (eIF4F) complex offers an appealing strategy to potentiate the effectiveness of existing cancer therapies and to overcome resistance to drugs such as BRAF inhibitors (BRAFi). Here, we identified and characterized the small molecule SBI-0640756 (SBI-756), a first-in-class inhibitor that targets eIF4G1 and disrupts the eIF4F complex. SBI-756 impaired the eIF4F complex assembly independently of mTOR and attenuated growth of BRAF-resistant and BRAF-independent melanomas. SBI-756 also suppressed AKT and NF-κB signaling, but small-molecule derivatives were identified that only marginally affected these pathways while still inhibiting eIF4F complex formation and melanoma growth, illustrating the potential for further structural and functional manipulation of SBI-756 as a drug lead. In the gene expression signature patterns elicited by SBI-756, DNA damage, and cell-cycle regulatory factors were prominent, with mutations in melanoma cells affecting these pathways conferring drug resistance. SBI-756 inhibited the growth of NRAS, BRAF, and NF1-mutant melanomas in vitro and delayed the onset and reduced the incidence of Nras/Ink4a melanomas in vivo. Furthermore, combining SBI-756 and a BRAFi attenuated the formation of BRAFi-resistant human tumors. Taken together, our findings show how SBI-756 abrogates the growth of BRAF-independent and BRAFi-resistant melanomas, offering a preclinical rationale to evaluate its antitumor effects in other cancers.
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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.