ArticleMolecular and cellular biochemistry2010
Regulating A549 cells growth by ASO inhibiting miRNA expression.
Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 52 citations in OpenAlex.
- miR-150 promotes human breast cancer growth and malignant behavior by targeting the pro-apoptotic purinergic P2X7 receptor.PloS one · 2013Trial
- miR-17: from developmental regulatory hub to molecular engine driving tumourigenesis.Frontiers in oncology · 2026Review
- Microfluidic Platforms for Ex Vivo and In Vivo Gene Therapy.Biosensors · 2025Review
- Nucleic acid drugs: recent progress and future perspectives.Signal transduction and targeted therapy · 2024Review
- Chemical modification patterns for microRNA therapeutic mimics: a structure-activity relationship (SAR) case-study on miR-200c.Nucleic acids research · 2024Article
- MicroRNA: Crucial modulator in purinergic signalling involved diseases.Purinergic signalling · 2023Review
- Regulation of Oncogenic Targets by Tumor-SuppressiveBiomedicines · 2021Article
- MicroRNA expression profiling and biomarker validation in treatment-naïve and drug resistant non-small cell lung cancer.Translational lung cancer research · 2021Article
- microRNAs targeting cellular cholesterol: implications for combating anticancer drug resistance.Genes & cancer · 2020Article
- Cisplatin decreases cyclin D2 expression via upregulating miR‑93 to inhibit lung adenocarcinoma cell growth.Molecular medicine reports · 2019Article
- Bioinformatic analysis of miR-4792 regulatesOncoTargets and therapy · 2019Article
- Engineering a customized nanodrug delivery system at the cellular level for targeted cancer therapy.Science China. Chemistry · 2018Article
- Interactions between anticancer active platinum complexes and non-coding RNAs/microRNAs.Non-coding RNA research · 2017Review
- Smad3-related miRNAs regulated oncogenic TRIB2 promoter activity to effectively suppress lung adenocarcinoma growth.Cell death & disease · 2016Article
- MicroRNA: a connecting road between apoptosis and cholesterol metabolism.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- High glucose concentration induces endothelial cell proliferation by regulating cyclin-D2-related miR-98.Journal of cellular and molecular medicine · 2016Article
- Role of microRNA-150 in solid tumors.Oncology letters · 2015Article
- Role of Exosomal Noncoding RNAs in Lung Carcinogenesis.BioMed research international · 2015Review
- Pharmaco-miR: linking microRNAs and drug effects.Briefings in bioinformatics · 2014Article
- Non-coding RNAs in lung cancer.Oncoscience · 2014Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) have a profound impact on cell processes, including proliferation, apoptosis, and stress responses. We aimed to explore the role of antisense oligonucleotide (ASO) to induce proliferation or apoptosis of A549 cancer cells by inhibiting the expression of miRNAs. After A549/HBE/293T cells were treated with ASO, cells proliferation/apoptosis, and their relevant oncogenes/tumor suppressor genes were detected by light and electron microscopy, real-time PCR, enzyme-linked immunosorbent assay, etc. The results showed that ASO could inhibit the expression of miRNAs effectively. miR-16, miR-17, miR-34a-c, and miR-125 served as tumor suppressor miRNAs, while miR-20, miR-106, and miR-150 acted as oncogenic miRNAs. Our results also indicated that miR-16/34a-c, miR-17-5p, miR-125, miR-106, and miR-150 were the upstream factors, which could regulate the expression of BCL-2, E2F1, E2F3, RB1, and P53, respectively. After A549 cells treated with ASO for 24 h and different concentrations of anti-cancer drug (cisplatin or demethylcantharidin) were added into culture medium, the results indicated the percentage of alive cells in group treated with both ASO-106 (or ASO-150) and anti-cancer drug was lower than that in group treated with ASO, or anti-cancer drug, or both ASO-16 (or ASO-34a) and anti-cancer drug. In conclusion, ASO (specific to oncogenic miRNAs) could induce A549 cells apoptosis by inhibiting oncogenic miRNAs, and could increase chemotherapy sensitivity of A549 cells to anti-cancer drug, which holds great promise to lung cancer therapy.
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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.