ArticleCell death & disease2020
Upregulation of KCNQ1OT1 promotes resistance to stereotactic body radiotherapy in lung adenocarcinoma by inducing ATG5/ATG12-mediated autophagy via miR-372-3p.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 74 citations in OpenAlex.
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- Long non-coding RNAs as key orchestrators of the tumor microenvironment in lung cancer.Frontiers in immunology · 2025Review
- Non-coding RNAs: Emerging contributors to chemoresistance in chronic myeloid leukemia.Leukemia research reports · 2025Review
- The regulatory role and therapeutic potential of long non-coding RNA in non-small cell lung cancer.Journal of Cancer · 2025Review
- Comprehensive review of LncRNA-mediated therapeutic resistance in non-small cell lung cancer.Cancer cell international · 2024Review
- Blocking ACSL6 Compromises Autophagy via FLI1-Mediated Downregulation of COLs to Radiosensitize Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- TGM2-Mediated Autophagy Contributes to the Radio-Resistance of Non-Small Cell Lung Cancer Stem-like Cells.Biomedicines · 2024Article
- Overexpression of ESYT3 improves radioimmune responses through activating cGAS-STING pathway in lung adenocarcinoma.Experimental hematology & oncology · 2024Article
- Exploring the enigma: history, present, and future of long non-coding RNAs in cancer.Discover oncology · 2024Review
- Comprehensive landscape and future perspective of long noncoding RNAs in non-small cell lung cancer: it takes a village.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Review
- MiRNAs in Lung Adenocarcinoma: Role, Diagnosis, Prognosis, and Therapy.International journal of molecular sciences · 2023Review
- Long non‑coding RNAs as potential therapeutic targets in non‑small cell lung cancer (Review).International journal of molecular medicine · 2023Review
- Regulation of autophagy gene expression and its implications in cancer.Journal of cell science · 2023Review
- Ion Channels as Potential Tools for the Diagnosis, Prognosis, and Treatment of HPV-Associated Cancers.Cells · 2023Review
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- A narrative review of genetic biomarkers in non-small cell lung cancer: an update and future perspectives.AME medical journal · 2023Article
- Screening microRNAs as potential prognostic biomarkers for lung adenocarcinoma.Annals of medicine · 2023Article
- Regulatory miRNAs in cancer cell recovery from therapy exposure and its implications as a novel therapeutic strategy for preventing disease recurrence.The Enzymes · 2023Article
- RNA m6A methyltransferase METTL14 promotes the procession of non-small cell lung cancer by targeted CSF1R.Thoracic cancer · 2023Article
- Introduction of long non-coding RNAs to regulate autophagy-associated therapy resistance in cancer.Molecular biology reports · 2022Review
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stereotactic body radiotherapy (SBRT) has emerged as a standard treatment for non-small-cell lung cancer. However, its therapeutic advantages are limited with the development of SBRT resistance. The SBRT-resistant cell lines (A549/IR and H1975/IR) were established after exposure with hypofractionated irradiation. The differential lncRNAs were screened by microarray assay, then the expression was detected in LUAD tumor tissues and cell lines by qPCR. The influence on radiation response was assessed via in vitro and in vivo assays, and autophagy levels were evaluated by western blot and transmission electron microscopy. Bioinformatics prediction and rescue experiments were used to identify the pathways underlying SBRT resistance. High expression of KCNQ1OT1 was identified in LUAD SBRT-resistant cells and tissues, positively associated with a large tumor, advanced clinical stage, and a lower response rate to concurrent therapy. KCNQ1OT1 depletion significantly resensitized A549/IR and H1975/IR cells to radiation by inhibiting autophagy, which could be attenuated by miR-372-3p knockdown. Furthermore, autophagy-related 5 (ATG5) and autophagy-related 12 (ATG12) were confirmed as direct targets of miR-372-3p. Restoration of either ATG5 or ATG12 abrogated miR-372-3p-mediated autophagy inhibition and radiosensitivity. Our data describe that KCNQ1OT1 is responsible for SBRT resistance in LUAD through induction of ATG5- and ATG12-dependent autophagy via sponging miR-372-3p, which would be a potential strategy to enhance the antitumor effects of radiotherapy in LUAD.
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