ArticleAging2020
LncRNA NEAT1/miR-129/Bcl-2 signaling axis contributes to HDAC inhibitor tolerance in nasopharyngeal cancer.
Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- The Oncogenic Role of Long Non-Coding RNABiology · 2026Review
- Clinical progress and functional modalities of HDAC inhibitor-based combination therapies in cancer treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- A fishnet between nasopharyngeal carcinoma and resistance: the competing endogenous RNA network.Current treatment options in oncology · 2025Review
- Exploring microRNA targeting as a promising approach for solid tumor treatment.Frontiers in oncology · 2025Review
- In-depth organic mass cytometry reveals differential contents of 3-hydroxybutanoic acid at the single-cell level.Nature communications · 2024Article
- The Histone Deacetylase Family: Structural Features and Application of Combined Computational Methods.Pharmaceuticals (Basel, Switzerland) · 2024Review
- The promising role of miRNAs in radioresistance and chemoresistance of nasopharyngeal carcinoma.Frontiers in oncology · 2024Review
- Non-coding RNA and drug resistance in head and neck cancer.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Role of long non-coding RNA in chemoradiotherapy resistance of nasopharyngeal carcinoma.Frontiers in oncology · 2024Review
- MicroRNA-Mediated Regulation of Histone-Modifying Enzymes in Cancer: Mechanisms and Therapeutic Implications.Biomolecules · 2023Review
- Circular RNA circ_0000741/miR-379-5p/TRIM14 signaling axis promotes HDAC inhibitor (SAHA) tolerance in glioblastoma.Metabolic brain disease · 2023Article
- Regulatory miRNAs in cancer cell recovery from therapy exposure and its implications as a novel therapeutic strategy for preventing disease recurrence.The Enzymes · 2023Article
- Review
- Regulatory role of miR-129 and miR-384-5p on apoptosis induced by oxygen and glucose deprivation in PC12 cell.Experimental brain research · 2022Article
- Emerging role of lncRNAs in drug resistance mechanisms in head and neck squamous cell carcinoma.Frontiers in oncology · 2022Review
- Role of Long Non-Coding RNA Polymorphisms in Cancer Chemotherapeutic Response.Journal of personalized medicine · 2021Review
- lncRNA NEAT1 regulates CYP1A2 and influences steroid-induced necrosis.Open life sciences · 2021Article
- NEAT1 as a competing endogenous RNA in tumorigenesis of various cancers: Role, mechanism and therapeutic potential.International journal of biological sciences · 2021Review
- LncRNA LHFPL3-AS1 Promotes Oral Squamous Cell Carcinoma Growth and Cisplatin Resistance Through Targeting miR-362-5p/CHSY1 Pathway.OncoTargets and therapy · 2021Article
- Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase inhibitors (HDACis) - based therapeutic drug tolerance is one of the principal factors of poor prognosis of patients with nasopharyngeal cancer (NPC). Mechanisms of tolerance to HDACis are not well understood. Nowadays, dysregulation of long non-coding RNAs (LncRNAs) and microRNAs (miRNAs) has been reported to provide beneficial or inhibitory effects in drug-tolerance in various cancers. Herein, we established the HDAC inhibitor (SAHA)-tolerant NPC cell sublines, which had decreased apoptosis in response to SAHA treatment. We observed that the expression of miR-129 was significantly reduced in SAHA-tolerant NPC cells. Manipulating the expression of miR-129 overcame SAHA tolerance, and enhanced the SAHA-induced apoptosis. In terms of miR-129 downregulation, we identified that NEAT1 suppresses miR-129 expression. NEAT1 was found to be upregulated in SAHA tolerance cells. The depletion of NEAT1 phenocopied the effect of miR-129 overexpression, which also enhanced SAHA-induced apoptosis. Bcl-2 was the downstream target of miR-129 and contributed to SAHA tolerance in NPC. Our in vivo xenograft experiment confirmed that the administration of miR-129 or inhibition of Bcl-2 overcame the SAHA tolerance in NPC. In conclusion, NEAT1 increases in NPC tissues and manages to facilitate SAHA tolerance by modulating the miR-129/Bcl-2 axis, providing novel therapeutic targets for NPC treatment.
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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.