ArticleJournal of cellular and molecular medicine2020
LncRNA HOTTIP facilitates the stemness of breast cancer via regulation of miR-148a-3p/WNT1 pathway.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 60 citations in OpenAlex.
- Article
- Identification and validation of a refined CAF-Associated diagnostic signature in breast cancer.Scientific reports · 2026Article
- Wnt/β-Catenin-mTOR-autophagy crosstalk in breast cancer: context-dependent control of tumor progression, immune suppression, and therapeutic resistance.Frontiers in immunology · 2026Review
- The long antisense non-coding RNA HOXA transcript at the distal tip (LncRNA HOTTIP) in health and disease: a comprehensive review and in silico analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Upregulation of HOTTIP and Its Potential Role in Monitoring Exercise Adaptation.International journal of molecular sciences · 2025Article
- Exploring the Role of LINC00115 in Esophageal Squamous Cell Carcinoma: Insights Into JAK1/STAT3 Pathway Activation and Metastatic Potential.JCO precision oncology · 2025Article
- Establishing a prognostic model with immune-related genes and investigating EPHB6 expression pattern in breast cancer.Scientific reports · 2025Article
- Long non-coding RNAs: Key regulators of stemness in breast cancer.Frontiers in cell and developmental biology · 2025Review
- Neuronal injury and hepatotoxicity: astrocytes and stellate cells convergence and their role in tissue repair.Frontiers in neuroscience · 2025Review
- Exploring the clinical potential of circulating LncRNAs in breast cancer: insights into primary signaling pathways and therapeutic interventions.Functional & integrative genomics · 2024Review
- Review
- Genetic variants of LncRNAs HOTTIP and MEG3 influence nasopharyngeal carcinoma susceptibility and clinicopathologic characteristics in the Southern Chinese population.Infectious agents and cancer · 2024Article
- LINC01806 Promotes Breast Cancer Growth and Metastasis via Sponging miR-1286 to Disinhibit ZEB1 Expression.Biochemical genetics · 2024Article
- The expression and biological role of complement C1s in esophageal squamous cell carcinoma.Open life sciences · 2024Article
- Article
- Long non-coding RNA HOX transcript antisense intergenic RNA depletion protects against alcoholic hepatitis through the microRNA-148a-3p/sphingosine 1-phosphate receptor 1 axis.Cell and tissue research · 2023Article
- Article
- Long non-coding RNAs in breast cancer stem cells.Medical oncology (Northwood, London, England) · 2023Review
- Sauchinone inhibits breast cancer cell proliferation through regulating microRNA-148a-3p/HER-2 axis.Thoracic cancer · 2023Article
- Mechanisms of Long Non-Coding RNA in Breast Cancer.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence suggests that dysregulation of long non-coding RNA (lncRNA) plays a key role in tumorigenesis. The lncRNA, HOXA transcript at the distal tip (HOTTIP), has been reported to be up-regulated in multiple cancers, including breast cancer, and is involved in various biological processes, including the maintenance of stemness. However, the biological function and underlying modulatory mechanism of HOTTIP in breast cancer stem cells (BCSCs) remains unknown. In this study, we found that HOTTIP was markedly up-regulated in BCSCs and had a positive correlation with breast cancer progression. Functional studies revealed that overexpression of HOTTIP markedly promoted cell clonogenicity, increased the expression of the stem cell markers, OCT4 and SOX2, and decreased the expression of the differentiation markers, CK14 and CK18, in breast cancer cells. Knockdown of HOTTIP inhibited the CSC-like properties of BCSCs. Consistently, depletion of HOTTIP suppressed tumour growth in a humanized model of breast cancer. Mechanistic studies demonstrated that HOTTIP directly binds to miR-148a-3p and inhibits the mediation of WNT1, which leads to inactivation of the Wnt/β-catenin signalling pathway. Our study is the first to report that HOTTIP regulates the CSC-like properties of BCSCs by as a molecular sponge for miR-148a-3p to increase WNT1 expression, offering a new target for breast cancer therapy.
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