ArticleNature communications2020
TRIB3-EGFR interaction promotes lung cancer progression and defines a therapeutic target.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 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
77 citing papers in PubMed, 111 citations in OpenAlex.
- TRIB3 Promotes Laryngeal Cancer Progression via Regulating Ubiquitination of PPARα.Biochemical genetics · 2026Article
- Glycocholic acid inhibits TRIB3-ID1 axis to acelerate colitis progression via suppressing intestinal stem cell renewal.Nature communications · 2026Article
- Glucose‑driven TRIB3 enhances the tumorigenic potential of colon cancer via the PI3K/AKT pathway.Molecular medicine reports · 2026Article
- Glutamine Deprivation Triggers Tribbles Homolog 3 Dependent G-Quadruplex Resolution to Maintain DNA Repair and Tumor Survival.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Exploring and experimental validation of SLC7A11 and ferroptosis related prognostic genes in non-small cell lung cancer using bulk RNA sequencing and single-cell RNA sequencing.Biology direct · 2026Article
- Unveiling TRIB3: A new mediator in MET-driven hepatocellular carcinoma progression: Editorial on "MET promotes hepatocellular carcinoma development through the promotion of TRIB3-mediated FOXO1 degradation".Clinical and molecular hepatology · 2026Article
- Calcium Phosphate Nanoparticle Delivery of siInternational journal of nanomedicine · 2026Article
- Cytoskeletal remodeling via CAMSAP3 downregulation drives resistance to osimertinib in NSCLC cells.Cell death & disease · 2025Article
- RAB40C recruiting TRIM21 facilitates the progression of hepatocellular carcinoma by stabilizing EGFR.Cell communication and signaling : CCS · 2025Article
- Activating NEDD4L suppresses EGFR-driven lung adenocarcinoma growth via facilitating EGFR proteasomal degradation.Journal of experimental & clinical cancer research : CR · 2025Article
- Splicing Shift of RAC1 Accelerates Tumorigenesis and Defines a Potent Therapeutic Target in Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Targeting the TRIB3-MYC axis in cancer: mechanistic insights and therapeutic disruption strategies.Investigational new drugs · 2025Review
- METTL14 induces ferroptosis to inhibit colorectal cancer progression by inhibiting TRIB3 via an m6A-YTHDF2-dependent manner.Journal of molecular histology · 2025Article
- MET promotes hepatocellular carcinoma development through the promotion of TRIB3-mediated FOXO1 degradation.Clinical and molecular hepatology · 2025Article
- A CMTM6 Nanobody Overcomes EGFR-TKI Resistance in Non-Small Cell Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Integrative proteogenomic characterization reveals therapeutic targets in poorly differentiated and anaplastic thyroid cancers.Nature communications · 2025Article
- Tribbles Pseudokinase 3 Converts Sorafenib Therapy to Neutrophil-Mediated Lung Metastasis in Hepatocellular Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- γδ T-cell autoresponses to ectopic membrane proteins: a new type of pattern recognition.Cellular & molecular immunology · 2025Article
- Discovery of a molecular glue for EGFR degradation.Oncogene · 2025Article
- Tribbles pseudokinase 3 drives cancer stemness in oral squamous cell carcinoma cells by supporting the expression levels of SOX2 and EGFR.International journal of molecular medicine · 2025Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High expression or aberrant activation of epidermal growth factor receptor (EGFR) is related to tumor progression and therapy resistance across cancer types, including non-small cell lung cancer (NSCLC). EGFR tyrosine kinase inhibitors (TKIs) are first-line therapy for NSCLC. However, patients eventually deteriorate after inevitable acquisition of EGFR TKI-resistant mutations, highlighting the need for therapeutics with alternative mechanisms of action. Here, we report that the elevated tribbles pseudokinase 3 (TRIB3) is positively associated with EGFR stability and NSCLC progression. TRIB3 interacts with EGFR and recruits PKCα to induce a Thr654 phosphorylation and WWP1-induced Lys689 ubiquitination in the EGFR juxtamembrane region, which enhances EGFR recycling, stability, downstream activity, and NSCLC stemness. Disturbing the TRIB3-EGFR interaction with a stapled peptide attenuates NSCLC progression by accelerating EGFR degradation and sensitizes NSCLC cells to chemotherapeutic agents. These findings indicate that targeting EGFR degradation is a previously unappreciated therapeutic option in EGFR-related NSCLC.
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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.