RESUMO
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 IC20, IC25, and IC10 concentrations when combined with EGCG in similar concentrations, synergistically decreased cell viability versus single treatments of both agents. Also, in combined treatments at IC20 and IC25 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 IC25, IC20, and IC10 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.
RESUMO
We aimed to investigate the possible anticancer effects of radiation in combination with 17-allylamino-17-demethoxy geldanamycin (17-AAG) and silver graphene quantum dot (SQD) in breast cancer (BC) cells. MCF-7 BC cells treated with, or without, different concentrations of 17-AAG and synthesized SQD and cellular viability detected. The growth inhibitory effects of low concentrations of 17-AAG with minimally toxic concentration of SQD in combination with 2 Gy of X-ray radiation were examined. The apoptosis induction assessed by acridine orange/ethedium bromide staining. Likewise, the levels of lactate, hydrogen peroxide (H2 O2 ), nitric oxide (NO) were evaluated. The relative gene expression levels of Bax and Bcl-2 were detected by real-time polymerase chain reaction and the Bax/Bcl-2 expression ratio was determined. Moreover, the protein expression of epidermal growth factor receptor (EGFR) was assessed by western blot analysis. Treatment with low concentrations of 17-AAG and SQD at a minimally toxic concentration promoted inhibition of BC cell growth and induced apoptosis. In addition, significant reduction in cell viability was seen in triple combination versus all double and single treatments. Indeed 17-AAG and SQD in combined with radiation significantly increased the H2 O2 and NO versus single and double treated cases. In addition, triple combination treatment showed decreased lactate level in compared tomonotherapies. EGFR protein expression levels were found to decreased in all double and triple combined cases versus single treatments. Additionally, in double and triple treatments, Bax/Bcl2 ratio were higher in compared to single treatments. Treatment with low concentrations of 17-AAG and SQD at a minimally toxic concentration tends to induce anticancer effects and increase the radiation effects when applied with 2 Gy of radiation versus radiation monotherapy.
