ArticleFrontiers of medicine2014
Reactive oxygen species generation is essential for cisplatin-induced accelerated senescence in hepatocellular carcinoma.
Article in Frontiers of medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 44 citations in OpenAlex.
- Modified citrus pectin modulates splenic immune responses and galectin expression following cisplatin treatment in Wistar rats.Journal of molecular histology · 2026Article
- The spatiotemporal heterogeneity of reactive oxygen species in the malignant transformation of viral hepatitis to hepatocellular carcinoma: a new insight.Cellular & molecular biology letters · 2025Review
- Persisting blood-brain barrier disruption following cisplatin treatment in a mouse model of chemotherapy-associated cognitive impairment.GeroScience · 2025Article
- Senolytics: charting a new course or enhancing existing anti-tumor therapies?Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Impact of targeting the platelet-activating factor and its receptor in cancer treatment.Military Medical Research · 2025Review
- Therapy-induced senescence through the redox lens.Redox biology · 2024Review
- Review
- Suppression of PI3K/Akt/mTOR Signaling Pathway and Antioxidant System and Reversal of Cancer Cells Resistance to Cisplatin under the Effect of Curcumin.Bulletin of experimental biology and medicine · 2022Article
- Review
- ATM at the crossroads of reactive oxygen species and autophagy.International journal of biological sciences · 2021Review
- Review
- The Dynamic Process and Its Dual Effects on Tumors of Therapy-Induced Senescence.Cancer management and research · 2020Review
- Screening potential mitochondria-targeting compounds from traditional Chinese medicines using a mitochondria-based centrifugal ultrafiltration/liquid chromatography/mass spectrometry method.Journal of pharmaceutical analysis · 2018Article
- p53 and metabolism: from mechanism to therapeutics.Oncotarget · 2018Review
- Identification of Four Oxidative Stress-Responsive MicroRNAs, miR-34a-5p, miR-1915-3p, miR-638, and miR-150-3p, in Hepatocellular Carcinoma.Oxidative medicine and cellular longevity · 2017Article
- Small molecule compounds that induce cellular senescence.Aging cell · 2016Review
- A Mechanism for the Temporal Potentiation of Genipin to the Cytotoxicity of Cisplatin in Colon Cancer Cells.International journal of medical sciences · 2016Article
- miR-34a induces cellular senescence via modulation of telomerase activity in human hepatocellular carcinoma by targeting FoxM1/c-Myc pathway.Oncotarget · 2015Article
- Systemic chemotherapy is modulated by platelet-activating factor-receptor agonists.Mediators of inflammation · 2015Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accelerated senescence is important because this process is involved in tumor suppression and has been induced by many chemotherapeutic agents. The platinum-based chemotherapeutic agent cisplatin displays a wide range of antitumor activities. However, the molecular mechanism of cisplatin-induced accelerated senescence in hepatocellular carcinoma (HCC) remains unclear. In the present study, the growth inhibitory effect of cisplatin on HepG2 and SMMC-7721 cells was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cellular senescence was then assessed by β-galactosidase assay. Senescence-related factors, including p53, p21, and p16, were evaluated by quantitative reverse transcription-polymerase chain reaction. Reactive oxygen species (ROS) was analyzed by flow cytometry. Our results revealed that cisplatin reduced the proliferation of HepG2 and SMMC-7721 cells in a dose- and time-dependent manner. Senescent phenotype observed in cisplatintreated hepatoma cells was dependent on p53 and p21 activation but not on p16 activation. Furthermore, cisplatininduced accelerated senescence depended on intracellular ROS generation. The ROS scavenger N-acetyl-L-cysteine also significantly suppressed the cisplatin-induced senescence of HepG2 and SMMC-7721 cells. In conclusion, our results revealed a functional link between intracellular ROS generation and cisplatin-induced accelerated senescence, and this link may be used as a potential target of HCC.
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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.