ArticleExperimental and therapeutic medicine2019
Cisplatin effect on head and neck squamous cell carcinoma cells is modulated by ERK1/2 protein kinases.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
- Unraveling the molecular landscape: an overview on gene expression, epigenetic alterations, and therapeutic challenges in head and neck squamous cell carcinoma.Molecular genetics and genomics : MGG · 2026Review
- Epigenetic Remodeling in Thyroid Cancer: New Dimensions of Targeted Therapy Through lncRNA Modulation.Current issues in molecular biology · 2025Article
- Combined Effect of Conventional Chemotherapy with Epigenetic Modulators on Glioblastoma.Genes · 2025Article
- Expression patterns and clinical significance of vasculogenic mimicry-related genes in patients with head and neck squamous cell carcinoma.Frontiers in immunology · 2025Article
- Hybrid Albumin-Decorated Lipid-Nanocarrier-Mediated Delivery of Polyphenol-RichInternational journal of molecular sciences · 2024Article
- Mass spectrometry-based proteomic analysis to characterize cisplatin induced early signaling events in head and neck squamous cell carcinoma.Molecular & cellular oncology · 2024Article
- Novel Bovine Serum Albumin-Decorated-Nanostructured Lipid Carriers Able to Modulate Apoptosis and Cell-Cycle Response in Ovarian, Breast, and Colon Tumoral Cells.Pharmaceutics · 2023Article
- [Galectin-1 knockdown inhibits proliferation, migration, invasion and promotes apoptosis of lung adenocarcinoma cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Maternal fish oil consumption has a negative impact on mammary gland tumorigenesis in C3(1) Tag mice offspring.European journal of nutrition · 2021Article
- Overview of Evidence-Based Chemotherapy for Oral Cancer: Focus on Drug Resistance Related to the Epithelial-Mesenchymal Transition.Biomolecules · 2021Review
- Resveratrol Modulation of Apoptosis and Cell Cycle Response to Cisplatin in Head and Neck Cancer Cell Lines.International journal of molecular sciences · 2021Article
- Synthesis and Anticancer Evaluation of New 1,3,4-Oxadiazole Derivatives.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Therapeutic Potential of the Natural Compound S-Adenosylmethionine as a Chemoprotective Synergistic Agent in Breast, and Head and Neck Cancer Treatment: Current Status of Research.International journal of molecular sciences · 2020Review
- The Effect of Resveratrol or Curcumin on Head and Neck Cancer Cells Sensitivity to the Cytotoxic Effects of Cisplatin.Nutrients · 2020Article
- Article
- Association of the Epithelial-Mesenchymal Transition (EMT) with Cisplatin Resistance.International journal of molecular sciences · 2020Review
- Highlights of the 3rd conference of the Romanian Association of Immuno-Dermatology and the 37th conference of the Romanian Society of Immunology held in Bucharest between September 19 and 22, 2019.Experimental and therapeutic medicine · 2019Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The extracellular signal-regulated kinases (ERKs) are key transducers of the extracellular signals into intracellular responses and represent major molecular players in tumorigenesis. The aim of this study was to determine how curcumin (CRM) used as an adjuvant supports the apoptotic process induced by a single chemical agent treatment (cisplatin-CisPT) on two head and neck squamous cell carcinoma cell lines (FaDu and PE/CA-PJ49) and the involvement of ERK1/2 and/or p53 activation in this process. Data have shown that the CisPt effect is potentiated by CRM. CRM induced an increase of p53 protein phosphorylation in both cell lines. CisPt decreased p53 protein phosphorylation in FaDu cells, but increased it in PE/CA-PJ49 cells. Data showed that the constitutive expression of activated ERK1/2 protein-kinase was different in the two analyzed tumor cell lines. ERK1/2 activation status was essential for both cell processes, proliferation and apoptosis induced by CisPt and/or CRM treatment on squamous cell carcinoma cells. Our data suggest that p53 phosphorylation in the apoptotic process induced by CRM treatment might require the involvement of ERK1/2. In this regard the CisPt treatment suggested that p53 phosphorylation is ERK1/2 independent in FaDu cells having a p53 gene deletion and ERK1/2 dependent in PE/CA-PJ49 cells having a p53 gene amplification. Moreover, in both tumor cell lines our results support the involvement of p53 phosphorylation-ERK1/2 activation-dependent in the apoptosis induced by combined treatments (CisPt and CRM). The use of CRM as adjuvant could increase the efficiency of chemotherapy by modulating cellular activation processes of ERK1/2 signaling pathways. In conclusion, the particular mode of intervention by which ERK1/2 might influence cell proliferation and/or apoptosis processes depends on the type of therapeutic agent, the cells' particularities, and the activation status of the ERK1/2.
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