ArticleRSC advances2018
Anti-tumor effect of HOTAIR-miR-613-SNAI2 axis through suppressing EMT and drug resistance in laryngeal squamous cell carcinoma.
Article in RSC advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Resistance-oriented immunometabolic circuits in laryngeal squamous cell carcinoma: glycolysis-lactate signaling, mitochondrial stress, and tumor-myeloid crosstalk.Frontiers in immunology · 2026Review
- Upregulation of ARHGAP18 by miR-613 Inhibits Cigarette Smoke Extract-Induced Apoptosis and Epithelial-Mesenchymal Transition in Bronchial Epithelial Cells.International journal of chronic obstructive pulmonary disease · 2025Article
- The role of HOTAIR in the modulation of resistance to anticancer therapy.Frontiers in molecular biosciences · 2024Review
- The lncRNA HOTAIR: a pleiotropic regulator of epithelial cell plasticity.Journal of experimental & clinical cancer research : CR · 2023Review
- The Role and Mechanism of Long Non-Coding RNA HOTAIR in the Oncogenesis, Diagnosis, and Treatment of Head and Neck Squamous Cell Carcinoma.Clinical Medicine Insights. Oncology · 2023Review
- Overview on Molecular Biomarkers for Laryngeal Cancer: Looking for New Answers to an Old Problem.Cancers · 2022Review
- Emerging role of lncRNAs in drug resistance mechanisms in head and neck squamous cell carcinoma.Frontiers in oncology · 2022Review
- Long non-coding RNA ANRIL promotes proliferation, clonogenicity, invasion and migration of laryngeal squamous cell carcinoma by regulating miR-181a/Snai2 axis.Regenerative therapy · 2019Article
- MiR-182 regulates cell proliferation and apoptosis in laryngeal squamous cell carcinoma by targeting the CRR9.Bioscience reports · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Laryngeal squamous cell carcinoma (LSCC) is the main pathological type of laryngeal cancer, which attacks the head and neck. Our present study aims to investigate the effect of long non-coding RNA (LncRNA) HOX transcript antisense RNA (HOTAIR) on epithelial mesenchymal transition (EMT) and drug resistance in LSCC. Firstly, the level of HOTAIR was found to be overexpressed in LSCC tissues compared with normal healthy tissues. Then, increased EMT and drug resistance were suppressed by specific HOTAIR shRNA effectively in LSCC cell lines. Besides, miR-613 was predicted to be a target of HOTAIR through bioinformatics analysis. Meanwhile, we found that a down-regulated level of miR-613 could be increased by HOTAIR shRNA and suppressed by LncRNA HOTAIR transfection in LSCC cells. The targeting relationship between miR-613 and HOTAIR was further demonstrated by a luciferase report assay. What is more, the inhibiting effect of HOTAIR shRNA on EMT and drug resistance was obviously abolished by the miR-613 inhibitor. Moreover, SNAI2, a critical regulator of EMT, was predicted as a target of miR-613 through bioinformatics analysis and luciferase report assays. As expected, the level of SNAI2 could be suppressed by HOTAIR shRNA and increased by the miR-613 inhibitor. Additionally, we discovered that SANI2 shRNA had similar inhibiting effect on EMT and drug resistance with HOTAIR shRNA in LSCC cells. Finally, the
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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.