ArticleCell cycle (Georgetown, Tex.)2016
DNA damage responsive miR-33b-3p promoted lung cancer cells survival and cisplatin resistance by targeting p21
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 63 citations in OpenAlex.
- Heterogeneous dual-channel and interpretable graph representation learning with global virtual nodes for microRNA-mediated drug sensitivity prediction.Molecular diversity · 2026Article
- Mitochondria-associated non-coding RNAs and their impact on drug resistance.Frontiers in pharmacology · 2025Review
- Proregenerative MicroRNAs to Repair the Damaged Heart.European cardiology · 2025Review
- DNA damage response-related ncRNAs as regulators of therapy resistance in cancer.Frontiers in pharmacology · 2024Review
- METTL3 depletion contributes to tumour progression and drug resistance via N6 methyladenosine-dependent mechanism in HR+HER2-breast cancer.Breast cancer research : BCR · 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
- Cell cycle-specific phosphorylation of p53 protein in A549 cells exposed to cisplatin and standardized air pollutants.Frontiers in physiology · 2023Article
- Review
- MicroRNAs as Predictors of Lung-Cancer Resistance and Sensitivity to Cisplatin.International journal of molecular sciences · 2022Review
- Crude extract ofBioMedicine · 2022Article
- Footprints of microRNAs in Cancer Biology.Biomedicines · 2021Review
- MicroRNA-based signatures impacting clinical course and biology of ovarian cancer: a miRNOmics study.Biomarker research · 2021Article
- Acetyl-11-keto-β-boswellic acid enhances the cisplatin sensitivity of non-small cell lung cancer cells through cell cycle arrest, apoptosis induction, and autophagy suppression via p21-dependent signaling pathway.Cell biology and toxicology · 2021Article
- ZNF674-AS1 antagonizes miR-423-3p to induce G0/G1 cell cycle arrest in non-small cell lung cancer cells.Cellular & molecular biology letters · 2021Article
- miR-33b-3p Acts as a Tumor Suppressor by TargetingFrontiers in oncology · 2021Article
- LncRNA PRNCR1 rs1456315 and CCAT2 rs6983267 Polymorphisms on 8q24 Associated with Lung Cancer.International journal of general medicine · 2021Article
- [Role of P21 in Resistance of Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2020Review
- Activation of Mitochondrial 2-Oxoglutarate Dehydrogenase by Cocarboxylase in Human Lung Adenocarcinoma Cells A549 Is p53/p21-Dependent and Impairs Cellular Redox State, Mimicking the Cisplatin Action.International journal of molecular sciences · 2020Article
- Knockdown of PDIA6 Inhibits Cell Proliferation and Enhances the Chemosensitivity in Gastric Cancer Cells.Cancer management and research · 2020Article
- The Role of the Cyclin Dependent Kinase Inhibitor p21Cancers · 2019Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin is the most potent and widespread used chemotherapy drug for lung cancer treatment. However, the development of resistance to cisplatin is a major obstacle in clinical therapy. The principal mechanism of cisplatin is the induction of DNA damage, thus the capability of DNA damage response (DDR) is a key factor that influences the cisplatin sensitivity of cancer cells. Recent advances have demonstrated that miRNAs (microRNAs) exerted critical roles in DNA damage response; nonetheless, the association between DNA damage responsive miRNAs and cisplatin resistance and its underlying molecular mechanism still require further investigation. The present study has attempted to identify differentially expressed miRNAs in cisplatin induced DNA damage response in lung cancer cells, and probe into the effects of the misexpressed miRNAs on cisplatin sensitivity. Deep sequencing showed that miR-33b-3p was dramatically down-regulated in cisplatin-induced DNA damage response in A549 cells; and ectopic expression of miR-33b-3p endowed the lung cancer cells with enhanced survival and decreased γH2A.X expression level under cisplatin treatment. Consistently, silencing of miR-33b-3p in the cisplatin-resistant A549/DDP cells evidently sensitized the cells to cisplatin. Furthermore, we identified CDKN1A (p21) as a functional target of miR-33b-3p, a critical regulator of G1/S checkpoint, which potentially mediated the protection effects of miR-33b-3p against cisplatin. In aggregate, our results suggested that miR-33b-3p modulated the cisplatin sensitivity of cancer cells might probably through impairing the DNA damage response. And the knowledge of the drug resistance conferred by miR-33b-3p has great clinical implications for improving the efficacy of chemotherapies for treating lung cancers.
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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.