ArticleCells, tissues, organs2022
LncRNA HOTAIR Promotes Chemoresistance by Facilitating Epithelial to Mesenchymal Transition through miR-29b/PTEN/PI3K Signaling in Cervical Cancer.
Article in Cells, tissues, organs, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 58 citations in OpenAlex.
- Therapy resistance-related ncRNAs in cervical cancer: biomarkers and therapeutic targets.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Review
- Mechanisms of Paclitaxel Resistance: Recent Advances and Future Perspectives.International journal of molecular sciences · 2026Review
- Pathogenic Mechanisms in Cervical Cancer: Energy Metabolism, Hypoxia and Therapy.Life (Basel, Switzerland) · 2026Review
- Reprogramming the tumor immune microenvironment in cervical cancer: synergy between radiotherapy and immunotherapy.Molecular cancer · 2026Review
- The CeRNA role of HOTAIR: sponging MiRs to promote chemoresistance.Molecular biology reports · 2026Review
- The role of long non-coding RNAs in therapy resistance of cervical cancer and therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- Unraveling the FGFR-RNA splicing axis: Mechanisms, oncogenic crosstalks and innovations for therapeutic purpose.Acta pharmaceutica Sinica. B · 2026Review
- Unraveling the mechanisms of LncRNAs in cervical cancer: a comprehensive review.Cell death discovery · 2025Review
- PTEN defects in cancer, from gene to protein molecular causes and therapeutic targets.Discover oncology · 2025Review
- Targeting epigenetic regulators as a promising avenue to overcome cancer therapy resistance.Signal transduction and targeted therapy · 2025Review
- LNP-encapsulated miRNA29b for corneal repair: A novel approach to combat fibrosis.Materials today. Bio · 2025Article
- LINC01871 facilitates cervical cancer cell migration and immune escape by targeting miR-873-3p/MAP3K2 axis.The Kaohsiung journal of medical sciences · 2025Article
- A Novel 167-Amino Acid Protein Encoded by CircPCSK6 Inhibits Intrahepatic Cholangiocarcinoma Progression via IKBα Ubiquitination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Exploring extracellular RNA as drivers of chemotherapy resistance in cancer.Molecular biology reports · 2025Review
- LncRNA-miRNA-mRNA regulatory axes as potential biomarkers in cervical cancer: a comprehensive overview.Molecular biology reports · 2025Review
- Long noncoding RNAs involved in therapeutic response: implications for cervical cancer drug resistance.Frontiers in oncology · 2025Review
- Unraveling the role of long non-coding RNAs in therapeutic resistance in acute myeloid leukemia: New prospects & challenges.Non-coding RNA research · 2024Review
- Evaluation of Long Non-coding RNA (LncRNA) in the Pathogenesis of Chemotherapy Resistance in Cervical Cancer: Diagnostic and Prognostic Approach.Molecular biotechnology · 2024Review
- Article
- Promising predictive molecular biomarkers for cervical cancer (Review).International journal of molecular medicine · 2024Review
Corrections and comments
- Erratum issuedErratum.2022
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNA HOTAIR has been revealed to participate in the tumorigenesis of various cancers. However, the mechanism of HOTAIR involvement in cervical cancer has not been identified. Hence, this study aimed to explore the oncogenic and chemoresistant roles of HOTAIR in cervical cancer, and its underlying mechanism. RT-PCR, Western blot, and Luciferase assay were employed to determine the relationship of HOTAIR with miR-29b and PTEN and to study the role of HOTAIR in cervical cancer. CCK8 assay, cell migration, and invasion assay were used to reveal the role of HOTAIR in cervical cancer cell proliferation and metastasis. The inhibitory dose of chemotherapeutics was determined by CCK8 assay using probit analysis. HOTAIR was found to bind with miR-29b, and a negative correlation existed between HOTAIR and miR-29b expression in cervical cancer cells. In addition, HOTAIR promoted the migration and proliferation of cervical cancer cell lines HeLa and Siha, showing effects opposite to miR-29b. Further, HOTAIR facilitated the resistance of both HeLa and Siha cells against cisplatin, paclitaxel and docetaxel, whereas miR-29 suppressed the resistance of both cervical cancer cells against the 3chemotherapeutics. In addition, HOTAIR enhanced epithelial-to-mesenchymal transition (EMT), while miR-29b exerted an inhibitory effect on EMT. In cervical cancer cells, miR-29b did not affect promoter methylation of PTEN but regulated PTEN expression by targeting SP1. Transfection of miR-29b mimics led to a significant downregulation of PI3K. HOTAIR promotes chemoresistance by facilitating EMT through the miR-29b/PTEN/PI3K axis in cervical 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.