ArticleCancer biology & therapy2016
Decreased MicroRNA-26a expression causes cisplatin resistance in human non-small cell lung cancer.
Article in Cancer biology & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- MicroRNA Expression Analysis and Biological Pathways in Chemoresistant Non-Small Cell Lung Cancer.Cancers · 2025Article
- miR-26a is a Key Therapeutic Target with Enormous Potential in the Diagnosis and Prognosis of Human Disease.Current medicinal chemistry · 2024Review
- P53‑microRNA interactions regulate the response of colorectal tumor cells to oxaliplatin under normoxic and hypoxic conditions.Oncology reports · 2023Article
- Regulating POLR3G by MicroRNA-26a-5p as a promising therapeutic target of lung cancer stemness and chemosensitivity.Non-coding RNA research · 2023Article
- Contribution of MicroRNAs in Chemoresistance to Cisplatin in the Top Five Deadliest Cancer: An Updated Review.Frontiers in pharmacology · 2022Review
- Application and Prospect of CRISPR/Cas9 Technology in Reversing Drug Resistance of Non-Small Cell Lung Cancer.Frontiers in pharmacology · 2022Review
- Exosomal microRNA-107 reverses chemotherapeutic drug resistance of gastric cancer cells through HMGA2/mTOR/P-gp pathway.BMC cancer · 2021Article
- Article
- miR-26a Reverses Multidrug Resistance in Osteosarcoma by Targeting MCL1.Frontiers in cell and developmental biology · 2021Article
- CEACAM6 promotes cisplatin resistance in lung adenocarcinoma and is regulated by microRNA-146a and microRNA-26a.Thoracic cancer · 2020Article
- High Mobility Group A (HMGA): Chromatin Nodes Controlled by a Knotty miRNA Network.International journal of molecular sciences · 2020Review
- miR-1269b Drives Cisplatin Resistance of Human Non-Small Cell Lung Cancer via Modulating the PTEN/PI3K/AKT Signaling Pathway.OncoTargets and therapy · 2020Article
- MicroRNA-26a inhibits multiple myeloma cell growth by suppressing cyclin-dependent kinase 6 expression.The Kaohsiung journal of medical sciences · 2019Article
- Annexin 1-nuclear factor-κB-microRNA-26a regulatory pathway in the metastasis of non-small cell lung cancer.Thoracic cancer · 2019Article
- MiR-16-1 Targeted Silences Far Upstream Element Binding Protein 1 to Advance the Chemosensitivity to Adriamycin in Gastric Cancer.Pathology oncology research : POR · 2018Article
- Tumor suppressive role of miR-569 in lung cancer.Oncology letters · 2018Article
- Review
- [MicroRNA-26a and Tumor].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2017Review
- The Fragment HMGA2-sh-3p20 from HMGA2 mRNA 3'UTR Promotes the Growth of Hepatoma Cells by Upregulating HMGA2.Scientific reports · 2017Article
- Interactions between anticancer active platinum complexes and non-coding RNAs/microRNAs.Non-coding RNA research · 2017Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundLung cancer is the most common cancer that is caused by perturbation of regulatory pathways rather than dysfunction of a single gene. Cisplatin (CDDP; cis-diamminedichloroplatinum II) is the first member of a class of platinum-containing anti-cancer medication, which binds to DNA and triggers apoptosis. CDDP-based chemotherapy is used to treat various types of cancers. However, the efficacy of CDDP in the treatment of non-small-cell lung cancer (NSCLC) is limited by acquired drug resistance. MicroRNAs have recently emerged as key regulators of cancers, and miR-26a is one of down-regulated miRNAs in A549/CDDPres cell line. This study aimed to investigate the role of miR-26a in CDDP resistance in NSCLC as well as the underlying mechanisms.
methodsIn this study, we analyzed expressional profiles of CDDP resistance-related mRNA, miRNA, and transcription factors (TF) that regulate miRNA expression in NSCLC. A549 cells were treated with CDDP, miR-26a mimic, or miR-26a inhibitor, and followed by biological analysis including drug sensitivity assay, colony formation assay, terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling (TUNEL) assay, and cell cycle analysis. Luciferase assay was used to determine the target of miR-26a. The regulation of miR-26a in Akt pathway was measured by western blot.
resultsHigh mobility group A (HMGA) 2 was identified as the target of miR-26a. Overexpression of miR-26a in A549 cells inhibited G1-S transition, increased cell death in response to CDDP treatment, and decreased the colony formation of A549 cells. MiR-26a significantly decreased the expression of E2F1, diminished Akt phosphorylation, and downregulated Bcl2 expression. Cell growth was suppressed by inhibiting HMGA2-mediated E2F1-Akt pathway.
conclusionMiR-26a is responsible for A549 cell sensitivity in the treatment of CDDP through regulating HMGA2-mediated E2F1-Akt pathway.
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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.