Bax induces cytochrome c release by multiple mechanisms in mitochondria from MCF7 cells

Gómez-Crisóstomo, Nancy Patricia; López‐Marure, Rebeca; Zapata, Estrella; Zazueta, Cecilia; Martínez-Abundis, Eduardo

doi:10.1007/s10863-013-9508-x

Cited by 42 publications

(27 citation statements)

References 34 publications

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“…These proteins are regulators of mitochondrial membrane permeability and intermembrane space protein efflux, according to the opposing fractions of the anti-apoptosis members and pro-apoptosis members (32,33). Bax accelerates programmed cell death and undergoes a conformational change that causes translocation to the mitochondrial membrane, leading to the release of cytochrome c, which then triggers apoptosis (34). Cordycepin enhanced the expression level of Bax and decreased the expression level of Bid in the present study.…”

supporting

confidence: 54%

Cordycepin induces apoptosis in human liver cancer HepG2 cells through extrinsic and intrinsic signaling pathways

Shao

Yan

et al. 2016

Oncology Letters

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Abstract. Cordycepin, also termed 3'-deoxyadenosine, is a nucleoside analogue from Cordyceps sinensis and has been reported to demonstrate numerous biological and pharmacological properties. Our previous study illustrated that the anti-tumor effect of cordycepin may be associated with apoptosis. In the present study, the apoptotic effect of cordycepin on HepG2 cells was investigated using 4' ,6-diamidino-2-phenylindole, tetraethylbenzimidazolylcarbocyanine iodide and propidium iodide staining analysis and flow cytometry. The results showed that cordycepin exhibited the ability to inhibit HepG2 cells in a time-and dose-dependent manner when cells produced typical apoptotic morphological changes, including chromatin condensation, the accumulation of sub-G1 cells and change mitochondrial permeability. A potential mechanism for cordycepin-induced apoptosis of human liver cancer HepG2 cells may occur through the extrinsic signaling pathway mediated by the transmembrane Fas-associated with death domain protein. Apoptosis was also associated with Bcl-2 family protein regulation, leading to altered mitochondrial membrane permeability and resulting in the release of cytochrome c into the cytosol. The activation of the caspase cascade is responsible for the execution of apoptosis. In conclusion, cordycepin-induced apoptosis in HepG2 cells involved the extrinsic and intrinsic signaling pathway and was primarily regulated by the Bcl-2 family proteins.

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supporting

confidence: 54%

Cordycepin induces apoptosis in human liver cancer HepG2 cells through extrinsic and intrinsic signaling pathways

Shao

Yan

et al. 2016

Oncology Letters

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“…Bax, a bcl2 family protein, interacts with bcl2 protein and induces apoptosis. Bax is reported to increase the opening of the mitochondrial voltagedependent anion channel, which leads to the loss in membrane potential and the release of cytochrome c. The increase in bax and cytochrome c is in accordance with the previous findings (Gómez et al, 2013). …”

Section: Discussionsupporting

confidence: 92%

Enhanced cytotoxic potential of Orthosiphon stamineus extract in MCF-7 cells through suppression of nucleolin and bcl2

Saravanan

Brindha

Sridharan

et al. 2017

Bangladesh J Pharmacol

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The aim of the present study was to analyze the anti-cancer effect of Orthosiphon stamineus leaf extract on MCF-7 cells. Ethyl acetate extract of the plant was eluted and pooled into 6 fractions based on their Rf values and the fractions were tested for cytotoxicity. Fraction 3 was found effective (IC50 = 28.5 µL/mL) and was subjected to LC-MS analysis which indicated the presence of biochanin, eleutherol and cinnamic acid. Further, cytotoxic effect of the fraction was confirmed in terms of nucleolin, bcl2, bax and cytochrome c expression in MCF-7 cells through RT-PCR where a marked decrease in nucleolin, bcl2 and increase in bax and cytochrome c were observed. The presence of eleutherol, a well-known anti-oxidant and anti-cancer agent, has been reported for the first time in O. stamineus. The anti-cancer activity of O. stamineus may be due to the presence of elutherol and cinnamic acid.Video Clip of Methodology:LC-MS analysis of Orthosiphon stamineus extract: 7 min 33 sec <a href="https://youtube.com/v/7Vop4epRjB0">Full Screen</a> <a href="https://youtube.com/watch?v=7Vop4epRjB0">Alternate</a>

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“…Taken together, these findings directly revealed that DSePA blocked high glucose-induced mitochondrial dysfunction. Bcl-2 family is thought to be important in regulation of Δψm and mitochondria-mediated apoptosis [21]. The balance between pro-apoptotic proteins (Bax, Bad, and Bid) and antiapoptotic proteins (Bcl-2 and Bcl-xL) decides the cells fate [22].…”

Section: Dsepa Blocks High Glucose-induced Mitochondrial Dysfunction mentioning

confidence: 99%

DSePA Antagonizes High Glucose-Induced Neurotoxicity: Evidences for DNA Damage-Mediated p53 Phosphorylation and MAPKs and AKT Pathways

Wang

et al. 2015

Mol Neurobiol

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Hyperglycemia as the major hallmark of diabetic neuropathy severely limited its therapeutic efficiency. Evidences have revealed that selenium (Se) as an essential trace element could effectively reduce the risk of neurological diseases. In the present study, 3,3'-diselenodipropionic acid (DSePA), a derivative of selenocystine, was employed to investigate its protective effect against high glucose-induced neurotoxicity in PC12 cells and evaluate the underlying mechanism. The results suggested that high glucose showed significant cytotoxicity through launching mitochondria-mediated apoptosis in PC12 cells, accompanied by poly (ADP-ribose) polymerase (PARP) cleavage, caspase activation, and mitochondrial dysfunction. Moreover, high glucose also triggered DNA damage and dysregulation of MAPKs and AKT pathways through reactive oxygen species (ROS) overproduction. p53 RNA interference partially suppressed high glucose-induced cytotoxicity and apoptosis, indicating the role of p53 in high glucose-induced signal. However, DSePA pretreatment effectively attenuated high glucose-induced cytotoxicity, inhibited the mitochondrial dysfunction through regulation of Bcl-2 family, and ultimately reversed high glucose-induced apoptotic cell death in PC12 cells. Attenuation of caspase activation, PARP cleavage, DNA damage, and ROS accumulation all confirmed its protective effects. Moreover, DSePA markedly alleviated the dysregulation of AKT and MAPKs pathways induced by high glucose. Our findings revealed that the strategy of using DSePA to antagonize high glucose-induced neurotoxicity may be a highly effective strategy in combating high glucose-mediated neurological diseases.

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Bax induces cytochrome c release by multiple mechanisms in mitochondria from MCF7 cells

Cited by 42 publications

References 34 publications

Cordycepin induces apoptosis in human liver cancer HepG2 cells through extrinsic and intrinsic signaling pathways

Cordycepin induces apoptosis in human liver cancer HepG2 cells through extrinsic and intrinsic signaling pathways

Enhanced cytotoxic potential of Orthosiphon stamineus extract in MCF-7 cells through suppression of nucleolin and bcl2

DSePA Antagonizes High Glucose-Induced Neurotoxicity: Evidences for DNA Damage-Mediated p53 Phosphorylation and MAPKs and AKT Pathways

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