ArticleBritish journal of cancer2014
MiR-224 promotes the chemoresistance of human lung adenocarcinoma cells to cisplatin via regulating G₁/S transition and apoptosis by targeting p21(WAF1/CIP1).
Article in British journal of cancer, 2014. 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 53 papers.
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Who cites it
53 citing papers in PubMed, 125 citations in OpenAlex.
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- T-box 2 expression is a useful indicator of the response to neoadjuvant chemotherapy for patients with locally advanced uterine cervical squamous cell carcinoma.Oncology letters · 2021Article
- Molecular Mechanisms of Chemoresistance Induced by Cisplatin in NSCLC Cancer Therapy.International journal of molecular sciences · 2021Review
- Meiotic nuclear divisions 1 (MND1) fuels cell cycle progression by activating a KLF6/E2F1 positive feedback loop in lung adenocarcinoma.Cancer communications (London, England) · 2021Article
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- 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
- Frontiers of MicroRNA Signature in Non-small Cell Lung Cancer.Frontiers in cell and developmental biology · 2021Review
- Circular RNA hsa_circ_0004872 inhibits gastric cancer progression via the miR-224/Smad4/ADAR1 successive regulatory circuit.Molecular cancer · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIncreasing evidence has shown that microRNAs (miRNAs) can serve as oncogenes and tumour suppressors to participate in tumour development. However, the roles of miRNAs in chemoresistance of human lung adenocarcinoma (LA) remain largely undefined.
methodsOn the basis of miRNA microarray data, miR-224 was identified as the most upregulated miRNA in cisplatin (DDP; cis-diamminedichloroplatinum II)-resistant A549 cells compared with parental A549 cells. The aim of our study was to investigate the roles of miR-224 in the formation of DDP-resistant phenotype of LA cells and its possible molecular mechanisms.
resultsHere we showed that miR-224 could promote the in vitro and in vivo DDP resistance of LA cells via regulating G1/S cell cycle transition and apoptosis. p21(WAF1/CIP1), a potent cyclin-dependent kinase inhibitor, was identified as the direct and functional target gene of miR-224. Overexpression of p21(WAF1/CIP1) could phenocopy the effect of miR-224 downregulation and silencing of p21(WAF1/CIP1) could partially reverse the effect of miR-224 downregulation on DDP resistance of DDP-resistant LA cells. In addition, miR-224 could affect the G1/S transition of cell cycle and apoptosis in LA cells through the p21(WAF1/CIP1)-pRb pathway and the intrinsic mitochondrial death pathway. Furthermore, miR-224 was found to be downregulated in DDP-responding LA tissues, and its expression was inversely correlated with p21(WAF1/CIP1). Multivariate analyses indicated that the status of miR-224 might be an independent prognostic factor for predicting the survival of LA patients.
conclusionsOur findings shed novel light on the roles of miR-224/p21(WAF1/CIP1) signalling in the DDP resistance of LA cells, and targeting it will be a potential strategic approach for reversing the DDP resistance in human LAs.
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