ArticleMolecular therapy : the journal of the American Society of Gene Therapy2022
Phosphorylation of TRIP13 at Y56 induces radiation resistance but sensitizes head and neck cancer to cetuximab.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Multi-omics analysis and functional validation reveal the oncogenic role of TRIP13.Frontiers in immunology · 2026Article
- Discovery of novel antimyeloma agents targeting TRIP13 by molecular modeling and bioassay.RSC medicinal chemistry · 2025Article
- Repeated ionizing radiation exposure induces TRIP13 expression, conferring radioresistance in lung cancer cells.Scientific reports · 2025Article
- TRIP13 regulates progression of gastric cancer through stabilising the expression of DDX21.Cell death & disease · 2024Article
- TRIP13 Plays an Important Role in the Sensitivity of Leukemia Cell Response to Sulforaphane Therapy.ACS omega · 2024Article
- Germline specific genes increase DNA double-strand break repair and radioresistance in lung adenocarcinoma cells.Cell death & disease · 2024Article
- Decoding the research landscape of drug resistance and therapeutic approaches in head and neck cancer: a bibliometric analysis from 2000 to 2023.Frontiers in pharmacology · 2024Article
- Identification of Tumor-SuppressiveCancers · 2023Article
- TRIP13 overexpression promotes gefitinib resistance in non‑small cell lung cancer via regulating autophagy and phosphorylation of the EGFR signaling pathway.Oncology reports · 2023Article
- Cytokines secreted by inflamed oral mucosa: implications for oral cancer progression.Oncogene · 2023Review
- Article
- MiRNA and Potential Prognostic Value in Non-Smoking Females with Lung Adenocarcinoma by High-Throughput Sequencing.International journal of general medicine · 2023Article
- FAM64A promotes HNSCC tumorigenesis by mediating transcriptional autoregulation of FOXM1.International journal of oral science · 2022Article
- DCZ0415, a small-molecule inhibitor targeting TRIP13, inhibits EMT and metastasis via inactivation of the FGFR4/STAT3 axis and the Wnt/β-catenin pathway in colorectal cancer.Molecular oncology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
Radiation therapy, a mainstay of treatment for head and neck cancer, is not always curative due to the development of treatment resistance; additionally, multi-institutional trials have questioned the efficacy of concurrent radiation with cetuximab, the epidermal growth factor receptor (EGFR) inhibitor. We unraveled a mechanism for radiation resistance; that is, radiation induces EGFR, which phosphorylates TRIP13 (thyroid hormone receptor interactor 13) on tyrosine 56. Phosphorylated (phospho-)TRIP13 promotes non-homologous end joining (NHEJ) repair to induce radiation resistance. NHEJ is the main repair pathway for radiation-induced DNA damage. Tumors expressing high TRIP13 do not respond to radiation but are sensitive to cetuximab or cetuximab combined with radiation. Suppression of phosphorylation of TRIP13 at Y56 abrogates these effects. These findings show that EGFR-mediated phosphorylation of TRIP13 at Y56 is a vital mechanism of radiation resistance. Notably, TRIP13-pY56 could be used to predict the response to radiation or cetuximab and could be explored as an actionable target.
Indexed as
Identifiers
What OpenQuestion holds
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.