The catechin flavonoid reduces proliferation and induces apoptosis of murine lymphoma cells LB02 through modulation of antiapoptotic proteins

Papademetrio, Daniela L.; Trabucchi, Aldana; Cavaliere, Victoria; Ricco, Rafael A.; Costantino, Susana N.; Wagner, Marcelo L.; Álvarez, Élida

doi:10.1590/s0102-695x2013005000025

Cited by 17 publications

(10 citation statements)

References 35 publications

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“…Thus, targets related to apoptosis are of prime interest in cancer therapy. Accumulating evidence suggests that flavonoid-induced apoptosis is characterized by nuclear condensation, disruption of mitochondrial membrane integrity, and up-regulation of apoptogenic proteins [ 35 , 36 ]. Here, our results demonstrate that HMF induced the intrinsic apoptosis pathway.…”

Section: Discussionmentioning

confidence: 99%

5-Hydroxy-7-Methoxyflavone Triggers Mitochondrial-Associated Cell Death via Reactive Oxygen Species Signaling in Human Colon Carcinoma Cells

et al. 2016

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Plant-derived compounds are an important source of clinically useful anti-cancer agents. Chrysin, a biologically active flavone found in many plants, has limited usage for cancer chemotherapeutics due to its poor oral bioavailability. 5-Hydroxy-7-methoxyflavone (HMF), an active natural chrysin derivative found in various plant sources, is known to modulate several biological activities. However, the mechanism underlying HMF-induced apoptotic cell death in human colorectal carcinoma cells in vitro is still unknown. Herein, HMF was shown to be capable of inducing cytotoxicity in HCT-116 cells and induced cell death in a dose-dependent manner. Treatment of HCT-116 cells with HMF caused DNA damage and triggered mitochondrial membrane perturbation accompanied by Cyt c release, down-regulation of Bcl-2, activation of BID and Bax, and caspase-3-mediated apoptosis. These results show that ROS generation by HMF was the crucial mediator behind ER stress induction, resulting in intracellular Ca2+ release, JNK phosphorylation, and activation of the mitochondrial apoptosis pathway. Furthermore, time course study also reveals that HMF treatment leads to increase in mitochondrial and cytosolic ROS generation and decrease in antioxidant enzymes expression. Temporal upregulation of IRE1-α expression and JNK phosphorylation was noticed after HMF treatment. These results were further confirmed by pre-treatment with the ROS scavenger N-acetyl-l-cysteine (NAC), which completely reversed the effects of HMF treatment by preventing lipid peroxidation, followed by abolishment of JNK phosphorylation and attenuation of apoptogenic marker proteins. These results emphasize that ROS generation by HMF treatment regulates the mitochondrial-mediated apoptotic signaling pathway in HCT-116 cells, demonstrating HMF as a promising pro-oxidant therapeutic candidate for targeting colorectal cancer.

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Section: Discussionmentioning

confidence: 99%

5-Hydroxy-7-Methoxyflavone Triggers Mitochondrial-Associated Cell Death via Reactive Oxygen Species Signaling in Human Colon Carcinoma Cells

et al. 2016

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“…Flavonoids in particular might be bound by tumor cell membrane receptors, then activate some caspases in the upstream position or initiator caspases such as caspase-2 and caspase-8 -caspase-12, and then stimulate another caspases in downstream position or effectors caspases including caspase-3, caspase-6 , and caspase-7 to apoptosis execution. As reported, flavonoid has been proven capable of decreasing the expression of Bcl2 and otherwise increasing Bax expression 24 . In the intrinsic pathway integrity of mitochondrial membrane stability is controlled by a balance between the antagonistic actions of the proapoptotic and antiapoptotic members of the Bcl-2 family 10,27 .…”

Section: Discussionmentioning

confidence: 79%

“…Flavonoids particularily are able to induce apoptosis mediated by the release of cytochrome-c to the cytosol, by processing of procaspase-9, and through a caspase-3-dependent mechanism 23 . Flavonoids decrease caspase-9 and increase cellular apoptosis by the increase in expression of Bax and decrease in Bcl-2 expression 24 . Flavonoids in particular might be bound by tumor cell membrane receptors, then activate some caspases in the upstream position or initiator caspases such as caspase-2 and caspase-8 -caspase-12, and then stimulate another caspases in downstream position or effectors caspases including caspase-3, caspase-6 , and caspase-7 to apoptosis execution.…”

Section: Discussionmentioning

confidence: 99%

Effect of Thyponium flageliforme in Combination with Curcuma zedoaria and Phyllanthus niruri in Expression of Protein Estrogen Receptor and Caspase-9 on Breast Cancer Mice

Widayati

Chodidjah

Nasihun

2018

Journal of Natural Remedies

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Introduction: Incidence of breast cancer is high and constitutes a significant cause of female mortality. One of breast cancer type is Estrogen and Progesteron Receptor (ER and PR) positive, therefore affected by estrogen and progesteron concentration. Treatment of Thyponium flageliforme in combination with Curcuma zedoaria, and Phyllanthus niruri (TCP) have been proven capable of inhibiting tumor cells proliferation. Objective: To evaluate the expression of protein estrogen receptor and caspase-9 in C3H mice were inoculated with adenocarcinoma cells. Methods: 18 mice were inoculated with one million cells of breast adenocarcinoma per mouse and assigned into three groups. TCP with dosage 85 and 125 mg were treated for 21 days to evaluate the expression of protein estrogen receptor and caspase-9 measured by immuno-histochemical staining. Results: Mann Whitney analysis demonstrated that expression of protein estrogen receptor and caspase-9 in TCP 125 was significant (p < 0.05). Conclusion: Expression of protein estrogen receptor was decreased and caspase-9 expression was increased by TCP administration.

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“…Studies showed catechin regulates apoptosis through downregulation of anti-apoptotic protein Bcl-2 and survivin, while upregulating pro-apoptotic protein Bax [24]. In the other hand, catechin suppresses cell proliferation by inhibiting nuclear factor κB (NF-κB) activation, vascular endothelial growth factor (VEGF) expression, and protecting from reactive oxygen species (ROS) stimulation [25][26][27].…”

Section: Modulation Of Catechin and Caffeine Concentration Affected Cmentioning

confidence: 99%

Cocoa extract has activity on selectively killing of breast cancer cells line

Tunjung-Sari

Mahriani

Tiningrum

et al. 2015

JTLS

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Effect of the cocoa crude extract on mortality of breast cancer cell lines i.e. MCF-7, T47D and normal cell (Vero), was observed. Crude cocoa extract prepared from a freshly dried cocoa bean that was containing 14% catechin and 0.6% caffeine. Catechin and caffeine content were modulated to 2-folds (28% catechin or 1.2% caffeine) and 3-folds (42% catechin or 1.8% caffeine) by adding pure compounds. Extracts were dissolved in dimethylsulfoxide (DMSO) at concentrations ranging from 200 to 1600 μg/ml. The positive control was doxorubicin (0.5-16 μg/ml in DMSO). Cell lines (MCF-7, T47D, and Vero) were incubated in test sample for 24h at 37°, prior to 3-(4,4-dimetylthiazole-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The absorbance of each well was measured at 550 nm, and lethal concentration (LC50) was calculated. The cocoa extract induced mortality of breast cancer cell lines but not in Vero cells. The effect on MCF-7 was greater than on T47D, given the LC50 was 1236 μg/ml (MCF-7) and 1893 μg/ml (T47D). Cytotoxic potential of cocoa extract was much lower than doxorubicin whose LC50 was 0,777 μg/ml (MCF-7) and 0,082 μg/ml (T47D). Increasing catechin content to 2-folds did not significantly affect LC50 value, but 3-folds catechin content reduced LC50 to 1021 μg/ml. Meanwhile increasing caffeine content to 2-folds significantly reduced LC50 to 750 μg/ml, however, 3-fold content resulted in slightly higher LC50 at 780 μg/ml. This indicates that cocoa extract have anti-cancer potential, and purification may improve this property.

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The catechin flavonoid reduces proliferation and induces apoptosis of murine lymphoma cells LB02 through modulation of antiapoptotic proteins

Cited by 17 publications

References 35 publications

5-Hydroxy-7-Methoxyflavone Triggers Mitochondrial-Associated Cell Death via Reactive Oxygen Species Signaling in Human Colon Carcinoma Cells

5-Hydroxy-7-Methoxyflavone Triggers Mitochondrial-Associated Cell Death via Reactive Oxygen Species Signaling in Human Colon Carcinoma Cells

Effect of Thyponium flageliforme in Combination with Curcuma zedoaria and Phyllanthus niruri in Expression of Protein Estrogen Receptor and Caspase-9 on Breast Cancer Mice

Cocoa extract has activity on selectively killing of breast cancer cells line

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