ArticleBioengineered2022
LINC01578 affects the radiation resistance of lung cancer cells through regulating microRNA-216b-5p/TBL1XR1 axis.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- TBL1XR1 Promotes Coronary Artery Disease by Regulating Triglyceride Metabolism via the PPAR Pathway.Cardiology research and practice · 2025Article
- FTO/m6A mediates miR-138-5p maturation and regulates gefitinib resistance of lung adenocarcinoma cells by miR-138-5p/LCN2 axis.BMC cancer · 2024Article
- Two decades of a protooncogene TBL1XR1: from a transcription modulator to cancer therapeutic target.Frontiers in oncology · 2024Review
- The art of war: using genetic insights to understand and harness radiation sensitivity in hematologic malignancies.Frontiers in oncology · 2024Review
- miR-216b-5p promotes late apoptosis/necroptosis in trastuzumab-resistant SK-BR-3 cells.Turkish journal of biology = Turk biyoloji dergisi · 2023Article
- A roadmap to cure CHD2-related disorders.Therapeutic advances in rare diseaseReview
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radiation resistance largely limits the survival of patients with non-small-cell lung cancer (NSCLC). To understand the mechanism underlying radiation resistance, we explored the influence of LINC01578 in radiation-resistant NSCLC cells. LINC01578, miR-216b-5p and Transducin (beta)-like 1 X-linked receptor 1 (TBL1XR1) expression was evaluated in patients with NSCLC, and their correlation with patients' prognosis was examined. Radiation-resistant NSCLC cell line (A549-RR) was induced and treated with oligonucleotide or plasmid transfection, and cell biological functions were captured. The interplay between LINC01578, miR-216b-5p and TBL1XR1 was clarified. NSCLC patients showed high LINC01578 and TBL1XR1 expression, and low miR-216b-5p expression, which was correlated to shorter patients' prognosis, respectively. LINC01578 or TBL1XR1 deficiency or miR-216b-5p elevation suppressed the functional activities of A549-RR cells. LINC01578 suppression elevated miR-216b-5p expression, consequently leading to the down-regulation of TBL1XR1. miR-216b-5p silencing or TBL1XR1 overexpression compromised LINC01578 knockdown's effects on radiation resistance of A549-RR cells. In brief, LINC01578 suppresses miR-216b-5p and enhances TBL1XR1 expression, thus to promote biological functions of radiation-resistant NSCLC cells.
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