Key result
Carboplatin plus EGCG synergistically reduces esophageal cancer cell viability vs monotherapy via caspase upregulation.
Why the study?
The study was conducted to evaluate the effects of combinatorial treatments with carboplatin and epigallocatechin-3-gallate on the KYSE-30 esophageal cancer cell line and elucidate the underlying mechanisms.
Does the combination of carboplatin and EGCG synergistically induce cytotoxicity in KYSE-30 esophageal cancer cells?
Does the combination of carboplatin and EGCG synergistically induce cytotoxicity in KYSE-30 esophageal cancer cells?
p-value: p=<0.05
The combination of carboplatin and EGCG synergistically promotes cytotoxicity and apoptosis in esophageal cancer cells in vitro, suggesting a potential strategy to enhance chemotherapy efficacy.
Premature for clinical use; leaves open whether EGCG-carboplatin synergy holds in animal or human esophageal cancer models.
Background and purpose: We aimed at evaluating the effects of combinatorial treatments with carboplatin and epigallocatechin-3-gallate (EGCG) on the KYSE-30 esophageal cancer (EC) cell line and elucidate the underlying mechanisms. Experimental approach: EC cells were harvested and exposed to increasing concentrations of carboplatin and EGCG to construct a dose-response plot. Cell inhibitory effects were assessed by the MTT method and apoptosis-related gene expression levels (caspases 8 and 9) and Bcl-2 mRNA were detected using real-time polymerase chain reaction. The lactate levels in the various treated cases were analyzed using the colorimetric assay kit. In addition, total antioxidant capacity was measured. Findings/Results: The results indicated that, following treatments with carboplatin in IC 20 , IC 25 , and IC 10 concentrations when combined with EGCG in similar concentrations, synergistically decreased cell viability versus single treatments of both agents. Also, in combined treatments at IC 20 and IC 25 of both agents the gene expression ratio of caspases 8 and 9 upregulated significantly compared to monotherapies ( P < 0.05). Bcl-2 gene expression ratios were decreased in double agents treated cells versus monotherapies. Following treatment of KYSE-30 cells with carboplatin and EGCG in double combinations, lactate levels were significantly decreased compared with the untreated cells and single treatments ( P < 0.05). Also, in IC 25 , IC 20 , and IC 10 concentrations of both agents the total antioxidant capacity levels were decreased versus monotherapies and untreated cells. Conclusion and implications: The presented study determined that treatment with carboplatin and EGCG was capable of promoting cytotoxicity in EC cells and inhibits the cancer progress. Combined treatments with low concentrations of carboplatin and EGCG may promote apoptosis induction and inhibit cell growth. These results confirmed the anticancer effects of carboplatin and EGCG and providing a base for additional use of EGCG to the EC treatment.
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Taghvaei et al. (2021) studied Esophageal cancer. Carboplatin and epigallocatechin-3-gallate (EGCG) combination vs. Single treatments (monotherapies) and untreated cells was evaluated on Cell viability and apoptosis-related gene expression (p=<0.05). Combined treatment with carboplatin and EGCG synergistically decreased cell viability and upregulated caspases 8 and 9 expression compared to monotherapies in esophageal cancer cells (P<0.05).
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