ArticleMedComm2023
TXNL4B regulates radioresistance by controlling the PRP3-mediated alternative splicing of FANCI.
Article in MedComm, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- FANCI promotes esophageal squamous cell carcinoma progression and cell cycle regulation and interacts with FANCD2.Journal of gastrointestinal oncology · 2026Article
- FANCI: from genome guardian to translational therapeutic target.Frontiers in oncology · 2026Review
- Alternative Splicing: Molecular Mechanisms, Biological Functions, Diseases, and Potential Therapeutic Targets.MedComm · 2025Review
- Knockdown of FANCI suppresses hepatocellular carcinoma development via the PI3K/Akt/GSK-3β pathway.Heliyon · 2025Article
- A Novel Metabolomic Aging Clock Predicting Health Outcomes and Its Genetic and Modifiable Factors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- High expression of SRSF1 facilitates osteosarcoma progression and unveils its potential mechanisms.BMC cancer · 2024Article
- TXNL4B regulates radioresistance by controlling the PRP3-mediated alternative splicing of FANCI.MedComm · 2023Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ionizing radiation (IR) has been extensively used for cancer therapy, but the radioresistance hinders and undermines the radiotherapy efficacy in clinics greatly. Here, we reported that the spliceosomal protein thioredoxin-like 4B (TXNL4B) is highly expressed in lung tissues from lung cancer patients with radiotherapy. Lung cancer cells with TXNL4B knockdown illustrate increased sensitivity to IR. Mechanistically, TXNL4B interacts with RNA processing factor 3 (PRP3) and co-localizes in the nucleus post-IR. Nuclear localization of PRP3 promotes the alternative splicing of the Fanconi anemia group I protein (FANCI) transcript variants, FANCI-12 and FANCI-13. PRP3 regulates alternative splicing of FANCI toward the two variants, FANCI-12 and FANCI-13. Radioresistance was greatly enhanced through the combination of PRP31 and PRP8, the critical components of core spliceosome promoted by PRP3. Notably, the inhibition of PRP3 to suppress the production of FANCI-12 would deprive PRP31 and PRP8 of such interaction. As a result, cell cycle G2/M arrest was induced, DNA damage repair was delayed, and radiosensitivity was improved. Collectively, our study highlights potential novel underlying mechanisms of the involvement of TXNL4B and alternative splicing in radioresistance. The results would benefit potential cancer radiotherapy.
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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.