ArticleMolecular carcinogenesis2015
Elevated expression of long intergenic non-coding RNA HOTAIR in a basal-like variant of MCF-7 breast cancer cells.
Article in Molecular carcinogenesis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Breast Cancer Chemoresistance: Insights into the Regulatory Role of lncRNA.International journal of molecular sciences · 2023Review
- HOTAIR: a potential metastatic, drug-resistant and prognostic regulator of breast cancer.Molecular cancer · 2023Review
- Long noncoding RNA (lncRNA) HOTAIR: Pathogenic roles and therapeutic opportunities in gastric cancer.Genes & diseases · 2022Review
- The Mechanisms of lncRNA-Mediated Multidrug Resistance and the Clinical Application Prospects of lncRNAs in Breast Cancer.Cancers · 2022Review
- Long Non-coding RNA HOTAIR in Central Nervous System Disorders: New Insights in Pathogenesis, Diagnosis, and Therapeutic Potential.Frontiers in molecular neuroscience · 2022Review
- The Role of lncRNAs in Rare Tumors with a Focus on HOX Transcript Antisense RNA (International journal of molecular sciences · 2021Review
- Current Knowledge of Long Non-Coding RNA HOTAIR in Breast Cancer Progression and Its Application.Life (Basel, Switzerland) · 2021Review
- Functional Interaction among lncRNA HOTAIR and MicroRNAs in Cancer and Other Human Diseases.Cancers · 2021Review
- LncRNA HOTAIR enhances breast cancer radioresistance through facilitating HSPA1A expression via sequestering miR-449b-5p.Thoracic cancer · 2020Article
- Long Non-Coding RNACancers · 2020Review
- Long Non-Coding RNA: Dual Effects on Breast Cancer Metastasis and Clinical Applications.Cancers · 2019Review
- Morphological and pathological features of basal-like breast cancer.Translational cancer research · 2019Review
- Knockdown of lncRNA-HOTAIR downregulates the drug-resistance of breast cancer cells to doxorubicin via the PI3K/AKT/mTOR signaling pathway.Experimental and therapeutic medicine · 2019Article
- The Epigenetics of Triple-Negative and Basal-Like Breast Cancer: Current Knowledge.Journal of breast cancer · 2018Review
- Polymorphisms of long non-coding RNA HOTAIR with breast cancer susceptibility and clinical outcomes for a southeast Chinese Han population.Oncotarget · 2018Article
- Induction of a novel isoform of the lncRNA HOTAIR in Claudin-low breast cancer cells attached to extracellular matrix.Molecular oncology · 2017Article
- Role of long non-coding RNA in tumor drug resistance.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Induction of HOXA9 expression in three-dimensional organotypic culture of the Claudin-low breast cancer cells.Oncotarget · 2016Article
- Long-range regulators of the lncRNA HOTAIR enhance its prognostic potential in breast cancer.Human molecular genetics · 2016Article
- Genetic variants of lncRNA HOTAIR and risk of epithelial ovarian cancer among Chinese women.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
Epigenetic regulation of gene expression is critical to phenotypic maintenance and transition of human breast cancer cells. HOX antisense intergenic RNA (HOTAIR) is a long intergenic non-coding RNA that epigenetically represses gene expression via recruitment of enhancer of zeste homolog 2 (EZH2), a histone methyltransferase. Elevated expression of HOTAIR promotes progression of breast cancer. In the current study we examined the expression and function of HOTAIR in MCF-7-TNR cells, a derivative of the luminal-like breast cancer cell line MCF-7 that acquired resistance to TNF-α-induced cell death. The expression of HOTAIR, markers of the luminal-like and basal-like subtypes, and growth were compared between MCF-7 and MCF-7-TNR cells. These variables were further assessed upon inhibition of HOTAIR, EZH2, p38 MAPK, and SRC kinase in MCF-7-TNR cells. When compared with MCF-7 cells, MCF-7-TNR cells exhibited an increase in the expression of HOTAIR, which correlated with characteristics of a luminal-like to basal-like transition as evidenced by dysregulated gene expression and accelerated growth. MCF-7-TNR cells exhibited reduced suppressive histone H3 lysine27 trimethylation on the HOTAIR promoter. Inhibition of HOTAIR and EZH2 attenuated the luminal-like to basal-like transition in terms of gene expression and growth in MCF-7-TNR cells. Inhibition of p38 and SRC diminished HOTAIR expression and the basal-like phenotype in MCF-7-TNR cells. HOTAIR was robustly expressed in the native basal-like breast cancer cells and inhibition of HOTAIR reduced the basal-like gene expression and growth. Our findings suggest HOTAIR-mediated regulation of gene expression and growth associated with the basal-like phenotype of breast cancer cells.
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