ArticlePloS one2014
p53-dependent activation of microRNA-34a in response to etoposide-induced DNA damage in osteosarcoma cell lines not impaired by dominant negative p53 expression.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Non-coding RNAs in drug and radiation resistance of bone and soft-tissue sarcoma: a systematic review.eLife · 2022Pooled it
- Cellular adaptations impact the biological activity of naphthalene diimide G-quadruplex ligands in ALT-positive osteosarcoma cells.Cell death & disease · 2025Article
- MicroRNAs: The Link between the Metabolic Syndrome and Oncogenesis.International journal of molecular sciences · 2021Review
- Advances in the role of miRNAs in the occurrence and development of osteosarcoma.Open medicine (Warsaw, Poland) · 2020Article
- MicroRNA-449b-5p Suppresses Proliferation, Migration, and Invasion of Osteosarcoma by Targeting c-Met.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Licochalcone A Suppresses the Proliferation of Osteosarcoma Cells through Autophagy and ATM-Chk2 Activation.Molecules (Basel, Switzerland) · 2019Article
- MicroRNA-504 modulates osteosarcoma cell chemoresistance to cisplatin by targeting p53.Oncology letters · 2019Article
- Interplay of non-coding RNAs and approved antimetabolites such as gemcitabine and pemetrexed in mesothelioma.Non-coding RNA research · 2018Review
- Relations between approved platinum drugs and non-coding RNAs in mesothelioma.Non-coding RNA research · 2018Review
- Honokiol suppresses proliferation and induces apoptosis via regulation of the miR‑21/PTEN/PI3K/AKT signaling pathway in human osteosarcoma cells.International journal of molecular medicine · 2018Article
- NOVA1 acts as an oncogene in osteosarcoma.American journal of translational research · 2017Article
- MicroRNAs, DNA Damage Response, and Cancer Treatment.International journal of molecular sciences · 2016Review
- Current state of phenolic and terpenoidal dietary factors and natural products as non-coding RNA/microRNA modulators for improved cancer therapy and prevention.Non-coding RNA research · 2016Review
- Loss-of-function screening to identify miRNAs involved in senescence: tumor suppressor activity of miRNA-335 and its new target CARF.Scientific reports · 2016Article
- Genetically engineered pre-microRNA-34a prodrug suppresses orthotopic osteosarcoma xenograft tumor growth via the induction of apoptosis and cell cycle arrest.Scientific reports · 2016Article
- Combination therapy with bioengineered miR-34a prodrug and doxorubicin synergistically suppresses osteosarcoma growth.Biochemical pharmacology · 2015Article
- MicroRNA-23a enhances migration and invasion through PTEN in osteosarcoma.Cancer gene therapy · 2015Article
- Micro(mi) RNA-34a targets protein phosphatase (PP)1γ to regulate DNA damage tolerance.Cell cycle (Georgetown, Tex.) · 2015Article
- Oncogenic and Circadian Effects of Small Molecules Directly and Indirectly Targeting the Core Circadian Clock.Integrative cancer therapiesArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteosarcoma (OS) is the most common primary malignant bone tumor and prevalently occurs in the second decade of life. Etoposide, a chemotherapeutic agent used in combined treatments of recurrent human OS, belongs to the topoisomerase inhibitor family and causes DNA breakage. In this study we evaluated the cascade of events determined by etoposide-induced DNA damage in OS cell lines with different p53 status focusing on methylation status and expression of miR-34a that modulate tumor cell growth and cell cycle progression. Wild-type p53 U2-OS cells and U2-OS cells expressing dominant-negative form of p53 (U2- OS175) were more sensitive to etoposide than p53-deficient MG63 and Saos-2 cells, showing increased levels of unmethylated miR-34a, reduced expression of CDK4 and cell cycle arrest in G1 phase. In contrast, MG63 and Saos-2 cell lines presented aberrant methylation of miR-34a promoter gene with no miR-34a induction after etoposide treatment, underlining the close connection between p53 expression and miR-34a methylation status. Consistently, in p53siRNA transfected U2-OS cells we observed loss of miR-34a induction after etoposide exposure associated with a partial gain of gene methylation and cell cycle progress towards G2/M phase. Our results suggest that the open and unmethylated conformation of the miR-34a gene may be regulated by p53 able to bind the gene promoter. In conclusion, cell response to etoposide-induced DNA damage was not compromised in cells with dominant-negative p53 expression.
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