Resveratrol Triggers Apoptosis Through Regulating Ceramide Metabolizing Genes in Human K562 Chronic Myeloid Leukemia Cells

Kartal, Melis; Saydam, Güray; Şahin, Fahri; Baran, Yusuf

doi:10.1080/01635581.2011.538485

Cited by 43 publications

(32 citation statements)

References 31 publications

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“…Inhibition of GCS and SK1 triggered apoptosis via leading to ceramide accumulation in imatinibresistant and imatinib-sensitive K562 CML cell lines [209]. Additionally, when we treated K562 human CML cell lines and HL60 human acute pro-myelocytic leukemia cell lines with resveratrol in combination with ceramide analog, GCS inhibitor, or SK1 inhibitor, apoptotic effects of resveratrol increased synergistically in the cells treated with resveratrol and ceramide combination, while the cells treated with resveratrol and GCS or SK1 combinations resisted to apoptosis as compared to the control group [210,211]. Furthermore, our studies also showed that GCS and SK1 inhibition in combination with nilotinib or dasatinib treatment synergistically triggers apoptosis in K562 and Meg01 human CML cell lines [212,213].…”

Section: Bioactive Sphingolipids In Apoptotic Pathwaysmentioning

confidence: 96%

Major apoptotic mechanisms and genes involved in apoptosis

et al. 2016

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As much as the cellular viability is important for the living organisms, the elimination of unnecessary or damaged cells has the opposite necessity for the maintenance of homeostasis in tissues, organs and the whole organism. Apoptosis, a type of cell death mechanism, is controlled by the interactions between several molecules and responsible for the elimination of unwanted cells from the body. Apoptosis can be triggered by intrinsically or extrinsically through death signals from the outside of the cell. Any abnormality in apoptosis process can cause various types of diseases from cancer to auto-immune diseases. Different gene families such as caspases, inhibitor of apoptosis proteins, B cell lymphoma (Bcl)-2 family of genes, tumor necrosis factor (TNF) receptor gene superfamily, or p53 gene are involved and/or collaborate in the process of apoptosis. In this review, we discuss the basic features of apoptosis and have focused on the gene families playing critical roles, activation/inactivation mechanisms, upstream/downstream effectors, and signaling pathways in apoptosis on the basis of cancer studies. In addition, novel apoptotic players such as miRNAs and sphingolipid family members in various kind of cancer are discussed.

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Section: Bioactive Sphingolipids In Apoptotic Pathwaysmentioning

confidence: 96%

Major apoptotic mechanisms and genes involved in apoptosis

et al. 2016

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“…The apoptosis in SW-872 human liposarcoma cells induced by quercetin was mediated through the activation of caspase-3, Bax, and Bak and then cleavage of PARP and downregulation of Bcl-2. 12 Kim et al showed that antiproliferative effect of quercetin is mediated via inhibition of PI-3 kinase in cancer cells. 24 Our results revealed that resveratrol treatment induced a dose-dependent increase in the percentage of cells in G0/G1 phase, which was accompanied by a corresponding reduction in the percentage of cells in S phase.…”

Section: Discussionmentioning

confidence: 99%

“…9,10 Resveratrol has been shown to induce apoptosis in a variety of cancers such as chronic myeloid leukemia (CML), acute myeloid leukemia (AML), breast, prostate, colon and lung cancers. [11][12][13] The exact mechanism of resveratrol mediated anticancer effect is not fully identified.…”

Section: Introductionmentioning

confidence: 99%

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Resveratrol and quercetin-induced apoptosis of human 232B4 chronic lymphocytic leukemia cells by activation of caspase-3 and cell cycle arrest

2013

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Chronic lymphocytic leukemia (CLL), defined by accumulation of pathogenic B cells, has a very complex biology due to various factors such as inherited, host, and enviromental factors. Recently, finding new therapeutic agents or development of novel treatment strategies have been paid attention. Resveratrol and quercetin, important phytoalexins found in many plants, have been reported to have cytotoxic effects on various types of cancer. In this study, we examined cytotoxic, cytostatic, and apoptotic effects of these two important phenolic compounds on 232B4 human CLL cells. Cytotoxic effects of resveratrol and quercetin were determined by MTT cell proliferation assay. Changes in caspase-3 enzyme activity were measured using caspase-3 colorimetric assay. Annexin V-FITC/PI double staining was performed to measure apoptotic cell population. Effects of resveratrol and quercetin on cell cycle profiles of CLL cells were investigated by flow cytometry. Treatment of CLL cells with resveratrol and quercetin caused dose dependent inhibition of cell proliferation and increased apoptotic cell population through induction of caspase-3 activity. Cell cycle analysis displayed cell cycle arrest mainly in G0/G1 for both polyphenols. Our data, in total, showed for the first time that resveratrol and quercetin might block CLL growth through inducing apoptosis and cell cycle arrest.

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“…Resveratrol aglycone has been reported to have anticancer and chemosensitizing activities against cancer cells; mechanisms of action for this have previously been proposed (1,(25)(26)(27)(28). Anticancer mechanisms of action for resveratrol, which have been described predominantly from in vitro studies, include the inhibition of transcription factors, kinases and other molecules involved in cell proliferation and survival.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol-3-O-glucuronide and resveratrol-4′-O-glucuronide reduce DNA strand breakage but not apoptosis in Jurkat T cells treated with camptothecin

Zunino

Storms

2017

Oncology Letters

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Abstract.Resveratrol has been reported to inhibit or induce DNA damage, depending upon the type of cell and the experimental conditions. Dietary resveratrol is present in the body predominantly as metabolites and limited data is available concerning the activities of these metabolic products. In the present study, physiologically obtainable levels of the resveratrol metabolites resveratrol-3-O-glucuronide, resveratrol-4'-O-glucuronide and resveratrol-3-O-sulfate were evaluated for their ability to protect Jurkat T cells against DNA damage induced by the topoisomerase I inhibitors camptothecin and topotecan. The cells were pretreated for 24 h with 10 µM resveratrol aglycone or each resveratrol metabolite prior to the induction of DNA damage with camptothecin or topotecan. In separate experiments, the cells were co-treated with resveratrol or its metabolites, and a topoisomerase I inhibitor. The detection of histone 2AX phosphorylation and terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) were used to determine DNA damage, and apoptosis was measured using an antibody against cleaved poly ADP-ribose polymerase. It was identified that pretreatment of the cells with resveratrol-3-O-glucuronide and resveratrol-4'-O-glucuronide reduced the mean fluorescence intensity of staining for DNA strand breaks following treatment with camptothecin, while the percentage of cells undergoing apoptosis was unchanged. However, pretreatment of the cells with resveratrol aglycone increased the DNA damage and apoptosis induced by the drugs. These results suggest that the glucuronide metabolites of resveratrol partially protected the cells from DNA damage, but did not influence the induction of cell death by camptothecin and topotecan. These data suggest that resveratrol aglycone treatment may be beneficial for treating types of cancer that have direct contact with resveratrol prior to its metabolism, including gastrointestinal cancers, which are routinely treated with topoisomerase I inhibitors.

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Resveratrol Triggers Apoptosis Through Regulating Ceramide Metabolizing Genes in Human K562 Chronic Myeloid Leukemia Cells

Cited by 43 publications

References 31 publications

Major apoptotic mechanisms and genes involved in apoptosis

Major apoptotic mechanisms and genes involved in apoptosis

Resveratrol and quercetin-induced apoptosis of human 232B4 chronic lymphocytic leukemia cells by activation of caspase-3 and cell cycle arrest

Resveratrol-3-O-glucuronide and resveratrol-4′-O-glucuronide reduce DNA strand breakage but not apoptosis in Jurkat T cells treated with camptothecin

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