ArticleJournal of the Korean Association of Oral and Maxillofacial Surgeons2016
The influence of p53 mutation status on the anti-cancer effect of cisplatin in oral squamous cell carcinoma cell lines.
Article in Journal of the Korean Association of Oral and Maxillofacial Surgeons, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Modulation ofInternational journal of molecular sciences · 2026Article
- Therapeutic Potential of Allomyrinasin in Oral Squamous Cell Carcinoma via Decreased NBC Activity.Pharmaceutics · 2026Article
- Epigenetic downregulation of the proapoptotic geneMolecular medicine reports · 2025Article
- Silencing E6/E7 Oncoproteins in SiHa Cells Treated with siRNAs and Oroxylum indicum Extracts Induced Apoptosis by Upregulating p53/pRb Pathways.Applied biochemistry and biotechnology · 2024Article
- Upregulation of MDR- and EMT-Related Molecules in Cisplatin-Resistant Human Oral Squamous Cell Carcinoma Cell Lines.International journal of molecular sciences · 2019Article
- The role of p53 status on the synergistic effect of CKD-602 and cisplatin on oral squamous cell carcinoma cell lines.Molecular biology reports · 2019Article
- High expression of TMEM40 contributes to progressive features of tongue squamous cell carcinoma.Oncology reports · 2019Article
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Abstract
objectivesThe purpose of this study was to evaluate the anti-cancer activity of cisplatin by studying its effects on cell viability and identifying the mechanisms underlying the induction of cell cycle arrest and apoptosis on oral squamous cell carcinoma (OSCC) cell lines with varying p53 mutation status. MATERIALS AND
methodsThree OSCC cell lines, YD-8 (p53 point mutation), YD-9 (p53 wild type), and YD-38 (p53 deletion) were used. To determine the cytotoxic effect of cisplatin, MTS assay was performed. The cell cycle alteration and apoptosis were analyzed using flow cytometry. Western blot analysis was used to detect the expression of cell cycle alteration- or apoptosis-related proteins as well as p53.
resultsCisplatin showed a time- and dose-dependent anti-proliferative effect in all cell lines. Cisplatin induced G2/M cell accumulation in the three cell lines after treatment with 0.5 and 1.0 µg/mL of cisplatin for 48 hours. The proportion of annexin V-FITC-stained cells increased following treatment with cisplatin. The apoptotic proportion was lower in the YD-38 cell line than in the YD-9 or YD-8 cell lines. Also, immunoblotting analysis indicated that p53 and p21 were detected only in YD-8 and YD-9 cell lines after cisplatin treatment.
conclusionIn this study, cisplatin showed anti-cancer effects via G2/M phase arrest and apoptosis, with some difference among OSCC cell lines. The mutation status of p53 might have influenced the difference observed among cell lines. Further studies on p53 mutation status are needed to understand the biological behavior and characteristics of OSCCs and to establish appropriate treatment.
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