Epigallocatechin gallate and sulforaphane combination treatment induce apoptosis in paclitaxel-resistant ovarian cancer cells through hTERT and Bcl-2 down-regulation

Chen, Huaping; Landen, Charles N.; Li, Yuanyuan; Alvarez, Ronald D.; Tollefsbol, Trygve O.

doi:10.1016/j.yexcr.2012.12.026

Cited by 98 publications

(70 citation statements)

References 28 publications

(29 reference statements)

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“…In order to confirm this finding, we performed western blot analysis of PARP-1 and pro-caspase-3 and −9. Proteolytic cleavage of specific proteins such as PARP-1 has been shown to occur in cells exposed to a number of apoptotic stimuli (23–25). EVOOE was found to induce apoptotic cell death only in T24 cells in a dose-dependent manner.…”

Section: Resultsmentioning

confidence: 99%

Extra-virgin olive oil phenols block cell cycle progression and modulate chemotherapeutic toxicity in bladder cancer cells

et al. 2016

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Epidemiological data indicate that the daily consumption of extra-virgin olive oil (EVOO), a common dietary habit of the Mediterranean area, lowers the incidence of certain types of cancer, in particular bladder neoplasm. The aim of the present study was to evaluate the antiproliferative activity of polyphenols extracted from EVOO on bladder cancer (BCa), and to clarify the biological mechanisms that trigger cell death. Furthermore, we also evaluated the ability of low doses of extra-virgin olive oil extract (EVOOE) to modulate the in vitro activity of paclitaxel or mitomycin, two antineoplastic drugs used in the management of different types of cancer. Our results showed that EVOOE significantly inhibited the proliferation and clonogenic ability of T24 and 5637 BCa cells in a dose-dependent manner. Furthermore, cell cycle analysis after EVOOE treatment showed a marked growth arrest prior to mitosis in the G2/M phase for both cell lines, with the subsequent induction of apoptosis only in the T24 cells. Notably, simultaneous treatment of mitomycin C and EVOOE reduced the drug cytotoxicity due to inhibition of ROS production. Conversely, the co-treatment of T24 cells with paclitaxel and the polyphenol extract strongly increased the apoptotic cell death at each tested concentration compared to paclitaxel alone. Our results support the epidemiological evidence indicating that olive oil consumption exerts health benefits and may represent a starting point for the development of new anticancer strategies.

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Section: Resultsmentioning

confidence: 99%

Extra-virgin olive oil phenols block cell cycle progression and modulate chemotherapeutic toxicity in bladder cancer cells

et al. 2016

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“…Interestingly, we also noticed that low concentrations of EGCG promoted the cell growth in both A549 and NCI-H460 cells. In fact, a few studies also obtained the proproliferation effect of EGCG in low concentrations, but without any intensive discussions (31,32). We considered that it was because of the inhibition of classical MAPK pathway by hsa-miR-125a-3p.…”

Section: Discussionmentioning

confidence: 99%

EGCG Enhances the Efficacy of Cisplatin by Downregulating hsa-miR-98-5p in NSCLC A549 Cells

Zhou

Wang

Feng

2014

Nutrition and Cancer

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In the current study, the enhanced efficacy of cisplatin caused by (-)-epigallocatechin-3-gallate (EGCG) in nonsmall cell lung cancer (NSCLC) A549 cells was observed. The tumor size was significantly smaller in vivo in the combination of cisplatin and EGCG group, as compared with cisplatin-only group. However, in NCI-H460 cells, another kind of NSCLC cells, the efficacy of cisplatin was antagonized by EGCG. MiRNA microarray showed that hsa-miR-98-5p and hsa-miR-125a-3p were differentially expressed after EGCG treatment in these 2 cell lines. After transfection of hsa-miR-98-5p inhibitor, the survival fraction of both A549 and NCI-H460 cells was decreased upon cisplatin treatment. Meanwhile, as a critical regulator in the cisplatin-induced apoptosis, p53 was elevated by silencing of hsa-miR-98-5p. These results suggested that EGCG inhibited the expression of hsa-miR-98-5p, followed by an increase of p53, thus the efficacy of cisplatin was enhanced. Bioinformatics analysis showed that hsa-miR-125a-3p might have a strong connection with classical MAPK pathway. Taken together, these findings indicate that hsa-miR-98-5p could be a potential target in clinical cisplatin treatment of NSCLC. The combination of EGCG and cisplatin might be an effective therapeutic strategy in treating some type of NSCLC, although the possibility of antagonistic interactions must also be taken into account.

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“…This dietary bioactive compound promotes apoptosis and prevents the continued proliferation of breast cancer cells through various mechanisms. For example, SFN can work well in conjunction with other compounds, thereby increasing the efficacy of programmed cell death and the regulation of epigenetic processes within many different cell lines [16,17]. Our lab has conducted a number of studies with regard to the epigenetic impact of SFN in conjunction of other dietary compounds in cancer and their ability to promote cancer cell death.…”

Section: Sulforaphane (Sfn) and Withaferin A (Wa)mentioning

confidence: 99%

Novel Combination of Withaferin A and Sulforaphane Inhibits Epigenetic Machinery, Cellular Viability and Induces Apoptosis of Breast Cancer Cells

Royston¹,

Udayakumar²,

Lewis³

et al. 2017

Preprint

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Abstract:With cancer often classified as a disease that has an important epigenetic component, natural compounds that have the ability to regulate the epigenome become ideal candidates for study. Humans have a complex diet, which illustrates the need to elucidate the mechanisms of interaction between these bioactive compounds in combination. The natural compounds withaferin A (WA), from the Indian winter cherry, and sulforaphane (SFN), from cruciferous vegetables, have numerous anti-cancer effects and some report their ability to regulate epigenetic processes. Our study is the first to investigate the combinatorial effects of low physiologically achievable concentrations of WA and SFN on breast cancer cell proliferation, histone deacetylase1 (HDAC1) and DNA methyltransferases (DNMTs). No adverse effects were observed on control cells at optimal concentrations. There was synergistic inhibition of cellular viability in MCF-7 cells and a greater induction of apoptosis with the combinatorial approach than with either compound administered alone in both MDA-MB-231 and MCF-7 cells. HDAC expression was down-regulated at multiple levels. Lastly, we determined the combined effects of these bioactive compounds on the pro-apoptotic BAX and anti-apoptotic BCL-2 and found decreases in BCL-2 and increases in BAX. Taken together, our findings demonstrate the ability of low concentrations of combinatorial WA and SFN to promote cancer cell death and regulate key epigenetic modifiers in human breast cancer cells.

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Epigallocatechin gallate and sulforaphane combination treatment induce apoptosis in paclitaxel-resistant ovarian cancer cells through hTERT and Bcl-2 down-regulation

Cited by 98 publications

References 28 publications

Extra-virgin olive oil phenols block cell cycle progression and modulate chemotherapeutic toxicity in bladder cancer cells

Extra-virgin olive oil phenols block cell cycle progression and modulate chemotherapeutic toxicity in bladder cancer cells

EGCG Enhances the Efficacy of Cisplatin by Downregulating hsa-miR-98-5p in NSCLC A549 Cells

Novel Combination of Withaferin A and Sulforaphane Inhibits Epigenetic Machinery, Cellular Viability and Induces Apoptosis of Breast Cancer Cells

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