ArticleBioengineered2020
Long non-coding RNA H19 regulates proliferation and doxorubicin resistance in MCF-7 cells by targeting PARP1.
Article in Bioengineered, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 42 citations in OpenAlex.
- Resistance to doxorubicin therapy in breast cancer cells could be attenuated by ligustilide: impact on autophagy and LncRNA H19.BMC complementary medicine and therapies · 2026Article
- Glycolysis-related lncRNA FTX upregulates YAP1 to facilitate colorectal cancer progression via sponging miR-215-3p.Scientific reports · 2025Article
- Interaction between lncRNAs and RNA-binding proteins (RBPs) influences DNA damage response in cancer chemoresistance.Molecular biology reports · 2024Review
- ncRNADrug: a database for validated and predicted ncRNAs associated with drug resistance and targeted by drugs.Nucleic acids research · 2024Article
- Review
- Harnessing the potential of long non-coding RNAs in breast cancer: from etiology to treatment resistance and clinical applications.Frontiers in oncology · 2024Review
- Novel Insights on Ferroptosis Modulation as Potential Strategy for Cancer Treatment: When Nature Kills.Antioxidants & redox signaling · 2024Review
- Association of altered metabolic profiles and long non-coding RNAs expression with disease severity in breast cancer patients: analysis byMetabolomics : Official journal of the Metabolomic Society · 2023Article
- Chitosan-based nanoscale systems for doxorubicin delivery: Exploring biomedical application in cancer therapy.Bioengineering & translational medicine · 2023Review
- LncRNA H19 Impairs Chemo and Radiotherapy in Tumorigenesis.International journal of molecular sciences · 2022Review
- Diabetes regulated anti-inflammatory lncRNA is overexpressed in triple-negative breast cancer and predicts chemoresistance and tumor recurrence.Bioengineered · 2022Article
- The Mechanisms of lncRNA-Mediated Multidrug Resistance and the Clinical Application Prospects of lncRNAs in Breast Cancer.Cancers · 2022Review
- Lectin galactoside-binding soluble 3 binding protein mediates methotrexate resistance in choriocarcinoma cell lines.Bioengineered · 2022Article
- Long intergenic non-protein coding RNA 1273 confers sorafenib resistance in hepatocellular carcinoma via regulation of methyltransferase 3.Bioengineered · 2022Article
- The role of lncRNA H19 in tumorigenesis and drug resistance of human Cancers.Frontiers in genetics · 2022Review
- Article
- Sitagliptin protects renal glomerular endothelial cells against high glucose-induced dysfunction and injury.Bioengineered · 2022Article
- Long non-coding RNA (LncRNA) CASC9/microRNA(miR)-590-3p/sine oculis homeobox 1 (SIX1)/NF-κB axis promotes proliferation and migration in breast cancer.Bioengineered · 2021Article
- Article
- Oncogenic role of early growth response-1 in liver cancer through the regulation of the microRNA-675/sestrin 3 and the Wnt/β-catenin signaling pathway.Bioengineered · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemoresistance is a major obstacle to effective breast cancer chemotherapy. However, the underlying molecular mechanisms remain unclear. The long noncoding RNA H19 (H19) is involved in various stages of tumorigenesis, however, its role in doxorubicin resistance remains unknown. The goal of this study was to evaluate the role of H19 in the development of doxorubicin-resistant breast cancer. Quantitative real-time PCR (qRT-PCR) analyzed H19 expression in chemotherapy-resistant and sensitive breast cancer tissues. Both knockdown and overexpression of H19 were used to assess the sensitivity to doxorubicin in breast cancer cells
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Registered trials
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.