ArticlePloS one2012
An in vivo C. elegans model system for screening EGFR-inhibiting anti-cancer drugs.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
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- Conserved Gαq-PLCβ-PKC signaling mediates trametinib resistance in BRAFbioRxiv : the preprint server for biology · 2025Article
- A Drug Discovery Pipeline for MAPK/ERK Pathway Inhibitors in Caenorhabditis elegans.Cancer research communications · 2024Article
- Uncovering the Molecular Pathways Implicated in the Anti-Cancer Activity of the Imidazoquinoxaline Derivative EAPB02303 Using aInternational journal of molecular sciences · 2024Article
- The tyrosine kinase inhibitor Gefitinib reducesmicroPublication biology · 2024Article
- Exploring the Potential of Lapatinib, Fulvestrant, and Paclitaxel Conjugated with Glycidylated PAMAM G4 Dendrimers for Cancer and Parasite Treatment.Molecules (Basel, Switzerland) · 2023Article
- Caenorhabditis elegans for research on cancer hallmarks.Disease models & mechanisms · 2023Article
- Development of a traditional Chinese medicine-based agent for the treatment of cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2022Article
- A survey of the kinome pharmacopeia reveals multiple scaffolds and targets for the development of novel anthelmintics.Scientific reports · 2021Article
- Drug discovery: Insights from the invertebrate Caenorhabditis elegans.Pharmacology research & perspectives · 2021Review
- Isoharringtonine Induces Apoptosis of Non-Small Cell Lung Cancer Cells in Tumorspheroids via the Intrinsic Pathway.Biomolecules · 2020Article
- Rab8 and Rabin8-Mediated Tumor Formation by Hyperactivated EGFR Signaling via FGFR Signaling.International journal of molecular sciences · 2020Article
- An approach using Caenorhabditis elegans screening novel targets to suppress tumour cell proliferation.Cell proliferation · 2020Article
- Anti-cancer effect of doxorubicin is mediated by downregulation of HMG-Co A reductase via inhibition of EGFR/Src pathway.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Harmine suppresses hyper-activated Ras-MAPK pathway by selectively targeting oncogenic mutated Ras/Raf inCancer cell international · 2019Article
- Caenorhabditis elegans: A Model System for Anti-Cancer Drug Discovery and Therapeutic Target Identification.Biomolecules & therapeutics · 2014Review
- Caenorhabditis elegans as a model for cancer research.Molecular & cellular oncologyReview
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The epidermal growth factor receptor (EGFR) is a well-established target for cancer treatment. EGFR tyrosine kinase (TK) inhibitors, such as gefinitib and erlotinib, have been developed as anti-cancer drugs. Although non-small cell lung carcinoma with an activating EGFR mutation, L858R, responds well to gefinitib and erlotinib, tumors with a doubly mutated EGFR, T790M-L858R, acquire resistance to these drugs. The C. elegans EGFR homolog LET-23 and its downstream signaling pathway have been studied extensively to provide insight into regulatory mechanisms conserved from C. elegans to humans. To develop an in vivo screening system for potential cancer drugs targeting specific EGFR mutants, we expressed three LET-23 chimeras in which the TK domain was replaced with either the human wild-type TK domain (LET-23::hEGFR-TK), a TK domain with the L858R mutation (LET-23::hEGFR-TK[L858R]), or a TK domain with the T790M-L858R mutations (LET-23::hEGFR-TK[T790M-L858R]) in C. elegans vulval cells using the let-23 promoter. The wild-type hEGFR-TK chimeric protein rescued the let-23 mutant phenotype, and the activating mutant hEGFR-TK chimeras induced a multivulva (Muv) phenotype in a wild-type C. elegans background. The anti-cancer drugs gefitinib and erlotinib suppressed the Muv phenotype in LET-23::hEGFR-TK[L858R]-expressing transgenic animals, but not in LET-23::hEGFR-TK[T790M-L858R] transgenic animals. As a pilot screen, 8,960 small chemicals were tested for Muv suppression, and AG1478 (an EGFR-TK inhibitor) and U0126 (a MEK inhibitor) were identified as potential inhibitors of EGFR-mediated biological function. In conclusion, transgenic C. elegans expressing chimeric LET-23::hEGFR-TK proteins are a model system that can be used in mutation-specific screens for new anti-cancer drugs.
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