ArticleOncogenesis2020
NRIP3 upregulation confers resistance to chemoradiotherapy in ESCC via RTF2 removal by accelerating ubiquitination and degradation of RTF2.
Article in Oncogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- A novel CT-based radiomics model for predicting response and prognosis of chemoradiotherapy in esophageal squamous cell carcinoma.Scientific reports · 2024Article
- The Mechanism of Ubiquitination or Deubiquitination Modifications in Regulating Solid Tumor Radiosensitivity.Biomedicines · 2023Review
- Article
- Targeting the mitochondrial calcium uniporter inhibits cancer progression and alleviates cisplatin resistance in esophageal squamous cell carcinoma.International journal of oncology · 2023Article
- Genomic alterations dissection revealedTranslational lung cancer research · 2023Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
Abstract
Esophageal squamous cell carcinoma (ESCC) is a common malignant cancer worldwide. Despite recent improvements in surgical techniques and adjuvant therapies, the prognosis of patients with advanced ESCC remains poor. Resistance to chemoradiotherapy (CRT) remains a major cause of treatment failure for advanced ESCC patients. Here, we report that NRIP3 (nuclear receptor interacting protein 3) promotes ESCC tumor cell growth and resistance to CRT in ESCC cells by increasing and binding to DDI1 (DNA-damage inducible 1 homolog 1) and RTF2 (homologous to Schizosaccharomyces pombe Rtf2), and accelerating the removal of RTF2, which is a key determinant for the ability of cells to manage replication stress. In addition, we found that NRIP3 could increase DDI1 expression via PPARα. The NRIP3-PPARα-DDI1-RTF2 axis represents a protective molecular pathway in ESCC cells that mediates resistance to replication stress signals induced by chemoradiotherapy. In addition, elevated NRIP3 is associated with the poor clinical outcome of ESCC patients receiving radiotherapy and/or cisplatin-based chemotherapy. Our study therefore reveals that NRIP3 is a prognostic factor in ESCC and could have some predictive value to select patients who benefit from CRT treatment. A common mechanism that protects ESCC tumor cells from DNA damage induced by CRT is also revealed in this study.
Identifiers
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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.