ArticleJournal of translational medicine2015
Estradiol induces HOTAIR levels via GPER-mediated miR-148a inhibition in breast cancer.
Article in Journal of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.
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Who cites it
69 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- HOTAIR as a diagnostic and prognostic biomarker of gastrointestinal cancers: an updated meta-analysis and bioinformatics analysis based on TCGA data.Bioscience reports · 2023Pooled it
- Insights into the regulation of the HOTAIR proximal promoter.Biochemical Society transactions · 2026Review
- Interrelation between lncRNA HOTAIR and EZH2 expression and progression free survival during endocrine treatment in breast cancer.BMC cancer · 2026Article
- Article
- Sexual dimorphism in cancer: molecular mechanisms and precision oncology perspectives.Biology of sex differences · 2026Review
- Endocrine therapy resistance of breast cancer: Important role of G protein-coupled estrogen receptor (GPER) and new therapeutic strategies.Genes & diseases · 2026Review
- Specific GPCRs Elicit Unique Extracellular Vesicle MiRNA Array Signatures: An Exploratory Study.bioRxiv : the preprint server for biology · 2025Article
- Integrin αvβ3 as a Non-Genomic Estrogen Receptor in Breast Cancer for Signaling Pathways and Crosstalk.Cells · 2025Review
- The Estrogen-Autophagy Axis: Insights into Cytoprotection and Therapeutic Potential in Cancer and Infection.International journal of molecular sciences · 2024Review
- An emerging link between lncRNAs and cancer sex dimorphism.Human genetics · 2024Review
- Estetrol/GPER/SERPINB2 transduction signaling inhibits the motility of triple-negative breast cancer cells.Journal of translational medicine · 2024Article
- Endocrine nuclear receptors and long non‑coding RNAs reciprocal regulation in cancer (Review).International journal of oncology · 2024Review
- Current progress and prospects for G protein-coupled estrogen receptor in triple-negative breast cancer.Frontiers in cell and developmental biology · 2024Review
- Roles of long noncoding RNA in triple-negative breast cancer.Cancer medicine · 2023Review
- Exploiting Long Non-Coding RNAs and Circular RNAs as Pharmacological Targets in Triple-Negative Breast Cancer Treatment.Cancers · 2023Review
- HOTAIR: a potential metastatic, drug-resistant and prognostic regulator of breast cancer.Molecular cancer · 2023Review
- Long noncoding RNA HOTAIR facilitates pulmonary vascular endothelial cell apoptosis via DNMT1 mediated hypermethylation of Bcl-2 promoter in COPD.Respiratory research · 2022Article
- Comparative G-Protein-Coupled Estrogen Receptor (GPER) Systems in Diabetic and Cancer Conditions: A Review.Molecules (Basel, Switzerland) · 2022Review
- The Role of miRNAs in Dexmedetomidine's Neuroprotective Effects against Brain Disorders.International journal of molecular sciences · 2022Review
- KCNQ1OT1 affects cell proliferation, invasion, and migration through a miR-34a / Notch3 axis in breast cancer.Environmental science and pollution research international · 2022Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HOTAIR plays an important role in the regulation of cancer cell proliferation and cancer invasion in breast cancer. The up-regulation of HOTAIR has been reported in both estrogen receptor (ER) positive and triple-negative (TN) breast cancer. It has been reported that HOTAIR is regulated by estrogen (E2) via ERs in ER-positive breast cancer. However, it is unknown how HOTAIR is regulated in TN breast cancer. In this study, we found that HOTAIR was increased in the peripheral blood mononuclear cells and cancer tissues from breast cancer patients, and was especially higher in patients with metastatic breast cancer. In addition, we found that estrogen promoted HOTAIR through its receptor GPER and estrogen-induced breast cancer cell migration was reversed by deleting HOTAIR in TN breast cancer cells MDA-MB-231and BT549. Furthermore, we identified that E2-GPER induces the level of HOTAIR through the suppression of miR-148a. miR-148a level was negatively correlated with HOTAIR level in breast cancer patients. After the mutation of the predicted miR-148a binding sites in HOTAIR, miR-148a had no effect on HOTAIR. In conclusion, our findings offer important new insights into the ability of estrogenic GPER signaling to increase the HOTAIR level by inhibiting miR-148a in breast cancer.
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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.