ArticleOncology letters2018
Lentivirus-mediated silencing of HOTAIR lncRNA restores gefitinib sensitivity by activating Bax/Caspase-3 and suppressing TGF-α/EGFR signaling in lung adenocarcinoma.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Vitamin D as an Epigenetic Regulator: A Hypothetical Mechanism for Cancer Prevention via Inhibition of Oncogenic lncRNA HOTAIR.International journal of molecular sciences · 2025Article
- Review
- Long Non-Coding RNAs as Emerging Targets in Lung Cancer.Cancers · 2023Review
- Comparison of linear versus macrocyclic gadolinium chelates in rat skeletal muscle.Northern clinics of Istanbul · 2022Article
- Identification of Prognostic Model Based on Immune-Related LncRNAs in Stage I-III Non-Small Cell Lung Cancer.Frontiers in oncology · 2021Article
- Critical role of HOX transcript antisense intergenic RNA (HOTAIR) in gliomas.Journal of molecular medicine (Berlin, Germany) · 2020Review
- miR-548e Sponged by ZFAS1 Regulates Metastasis and Cisplatin Resistance of OC by Targeting CXCR4 and let-7a/BCL-XL/S Signaling Axis.Molecular therapy. Nucleic acids · 2020Article
- LncRNAs Act as a Link between Chronic Liver Disease and Hepatocellular Carcinoma.International journal of molecular sciences · 2020Review
- Role of downregulated ADARB1 in lung squamous cell carcinoma.Molecular medicine reports · 2020Article
- Knockdown of Long Non-Coding RNACancer management and research · 2020Article
- Deregulated lncRNA expression profile in the mouse lung adenocarcinomas with KRAS-G12D mutation and P53 knockout.Journal of cellular and molecular medicine · 2019Article
- LINC01093 Upregulation Protects against Alcoholic Hepatitis through Inhibition of NF-κB Signaling Pathway.Molecular therapy. Nucleic acids · 2019Article
- Long non‑coding RNAs in lung cancer: Regulation patterns, biologic function and diagnosis implications (Review).International journal of oncology · 2019Review
- Long noncoding RNA GAS5 silencing inhibits the expression of KCNQ3 by sponging miR-135a-5p to prevent the progression of epilepsy.The Kaohsiung journal of medical sciences · 2019Article
- Recent Progress in Characterizing Long Noncoding RNAs in Cancer Drug Resistance.Journal of Cancer · 2019Review
- The roles of lncRNA in hepatic fibrosis.Cell & bioscience · 2018Review
- lncRNA ROR Promotes Gastric Cancer Drug Resistance.Cancer control : journal of the Moffitt Cancer CenterArticle
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secondary resistance is a major limitation in the efficacy of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor treatment of lung cancer. Previous studies have shown that expression of the long non-coding RNA HOX transcript antisense RNA (HOTAIR) is upregulated in lung cancer, which is correlated with metastasis and poor prognosis. However, the precise role of HOTAIR and its effects on gefitinib resistance in human lung adenocarcinoma are not known. To address this issue, in the present study we established a gefitinib-resistant (R)PC-9 human lung adenocarcinoma cell line and examined cell viability with the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. We found that gefitinib concentrations <10 µM inhibited the viability of PC-9 but not RPC-9 cells in a dose-dependent manner. Lentivirus-mediated HOTAIR RNA interference induced cell apoptosis and S-phase arrest, as determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling and flow cytometry. Consistent with these observations, HOTAIR suppression was associated with tumor shrinkage and restoration of gefitinib sensitivity in RPC-9 xenograft mice. Immunohistochemical analyses and western blot revealed that HOTAIR silencing resulted in the upregulation of B cell lymphoma 2-associated X protein (Bax), Caspase-3 and transforming growth factor α (TGF-α) and downregulation of EGFR and B cell lymphoma 2 (Bcl-2) levels. These results indicate that HOTAIR normally prevents the activation of Bax/Caspase-3 while inducing TGF-α/EGFR signaling. Thus, targeting HOTAIR may be a novel therapeutic strategy for treating gefitinib-resistant lung adenocarcinoma.
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