Modulation of cisplatin cytotoxic activity against leiomyosarcoma cells by epigallocatechin-3-gallate

Dhima, Irida; Peschos, Dimitrios; Simos, Yannis V.; Gkiouli, Maria; Palatianou, Maria; Ragos, Vasileios; Kalfakakou, Vasiliki; Evangelou, Angelos; Karkabounas, Spyridon

doi:10.1080/14786419.2017.1343318

Cited by 6 publications

(7 citation statements)

References 22 publications

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Section: Discussionsupporting

confidence: 55%

“…The synergistic effects of other chemotherapy drugs with Gallic acid derivative have also been reported in a study ( 15 ). Dhima et al have shown pre-treatment with epigallocatechin-3-gallate (EGCG) sensitised leiomyosarcoma cells to cisplatin ( 15 ). Overall, synergistic combinations of herbal medicines and chemotherapy drugs may use for enhancing efficacy, reducing side effects, immune modulation, and abrogating drug resistance ( 13 ).…”

Section: Discussionsupporting

confidence: 55%

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Synergistic Effects of Lauryl Gallate and Tamoxifen on Human Breast Cancer Cell

Samani¹,

Farrokhi²,

Tabatabaee³

et al. 2020

ijph

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Background: Tamoxifen (TAM) is widely used for adjuvant therapy in breast cancer patients. Tamoxifen therapy may lead to serious side effects. Anti-apoptotic substances in combination with chemotherapy drugs can result in additive or synergistic effects. Lauryl gallate (LG), a Gallic acid derivative, has been proven to inhibit tumor growth, without affecting normal cells. This study aimed to investigate the synergistic effect of TAM and LG in breast cancer cell line (MCF-7). Methods: In this experimental study, performed in ShahreKord University of Medical Science, Iran in 2017, the MCF-7 cells were treated by final concentrations of 10 μM TAM alone, and in combination with 200 μM of LG. We also used EX-527, as SIRT-1 inhibitor to examine the role of SIRT1 in cell apoptosis. BCL-2 and SIRT1 gene expression were measured by real-time PCR method, and cell apoptosis was investigated by flow cytometry. Results: Tamoxifen alone and in combination with LG decreased BCL-2 expression 2.64±0.75 and 6.38±1.9 fold, respectively, after 48 h (P<0.05). SIRT1 expression was increased 1.67±0.22 and 2.47±0.34 - fold by TAM alone and in combination with LG, respectively (P<0.05). TAM alone and in combination with LG increased the percentage of apoptotic cells 15.79±2.81 and 60.67±6.23 percent, respectively after 48 h (P<0.001). Conclusion: The combination of LG and TAM is more effective for induction of apoptosis of breast cancer cells, compared to individual use of each. Thus, our data pave the way for new therapeutic options for suppressing breast cancer growth.

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Section: Discussionsupporting

confidence: 55%

Section: Discussionsupporting

confidence: 55%

Synergistic Effects of Lauryl Gallate and Tamoxifen on Human Breast Cancer Cell

Samani¹,

Farrokhi²,

Tabatabaee³

et al. 2020

ijph

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“…28 In this direction, we have recently shown that pretreatment with EGCG sensitizes LMS cells to cisplatin by enhancing the drug’s apoptotic effect without modifying the S-phase cell cycle arrest. 22…”

Section: Discussionmentioning

confidence: 99%

“…Induction of apoptosis was estimated with Annexin V-FITC and propidium iodide staining as previously described. 22 Briefly, LMS cells were seeded into 6-well plates at a density of 6 × 10 4 cells/well for 24 hours with or without addition of the CRV. The medium was removed, and the cells were then incubated additionally for 48 hours with fresh medium supplemented with the IC 50 of cisplatin, estimated by means of the MTT assay.…”

Section: Quantification Of Apoptosismentioning

confidence: 99%

“…[19][20][21] We have previously shown that pretreatment of leiomyosarcoma (LMS) cells with epigallocatechin gallate (EGCG) sensitizes cells to cisplatin. 22 The aim of the present work was to evaluate the effects of curcumin on cisplatin cytotoxic activity in a series of in vitro and in vivo experiments to discover less toxic but equally effective methods to induce cancer cell death.…”

Section: Introductionmentioning

confidence: 99%

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Curcumin Acts as a Chemosensitizer for Leiomyosarcoma Cells In Vitro But Fails to Mediate Antioxidant Enzyme Activity in Cisplatin-Induced Experimental Nephrotoxicity in Rats

et al. 2019

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Background. Cisplatin (cis-diamminedichloroplatinum) is a widely used chemotherapeutic agent for the treatment of various cancers. Although it represents an effective regimen, its application is accompanied by side effects to normal tissues, especially to the kidneys. Cisplatin generates free radicals and impairs the function of antioxidant enzymes. Modulation of cisplatin-induced oxidative stress by specific antioxidant molecules represents an attractive approach to minimize side effects. Methods. We studied the ability of curcumin to sensitize leiomyosarcoma (LMS) cells to cisplatin. Assays for cell proliferation, mitochondrial function, induction of apoptosis, and cell cycle arrest were performed using various concentrations of cisplatin and a concentration of curcumin that caused a nonsignificant reduction in cell viability. Moreover, the effect of curcumin was examined against cisplatin-induced experimental nephrotoxicity. Renal injury was assessed by measuring serum creatinine, blood urea nitrogen (BUN), and the kidney’s relative weight. Oxidative stress was measured by means of enzymatic activities of superoxide dismutase and glutathione peroxidase in the rats’ blood and malondialdehyde levels in rats’ urine. Results. In our study, we found that curcumin sensitizes LMS cells to cisplatin by enhancing apoptosis and impairing mitochondrial function. In an in vivo model of cisplatin-induced experimental nephrotoxicity, intraperitoneal administration of curcumin failed to preserve blood’s antioxidant enzyme activity and decrease lipid peroxidation. Nevertheless, curcumin was able to protect nephrons’ histology from cisplatin’s toxic effect. Conclusion. Our results showed that curcumin can act as chemosensitizer, but its role as an adjunctive cisplatin-induced oxidative stress inhibitor requires further dose-finding studies to maximize the effectiveness of chemotherapy.

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