MMPT as a reactive oxygen species generator induces apoptosis via the depletion of intracellular GSH contents in A549 cells

Zhao, Yaofeng; Zhang, Cui; Suo, Yourui

doi:10.1016/j.ejphar.2012.05.003

Cited by 21 publications

(12 citation statements)

References 34 publications

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“…5(D)) by the virtue of MMP loss which is a prime characteristic of apoptosis, while the untreated control cells showed high green fluorescence indicating the healthy mitochondria. Our observations were supported by an earlier report emphasizing the apoptotic cell death induced by MMP loss in A549 cell line [54].…”

Section: Anticancer Potentialsupporting

confidence: 93%

Biogenic silver nanoparticles from Abutilon indicum: Their antioxidant, antibacterial and cytotoxic effects in vitro

Mata

Nakkala

Rani

2015

Colloids and Surfaces B: Biointerfaces

139

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Section: Anticancer Potentialsupporting

confidence: 93%

Biogenic silver nanoparticles from Abutilon indicum: Their antioxidant, antibacterial and cytotoxic effects in vitro

Mata

Nakkala

Rani

2015

Colloids and Surfaces B: Biointerfaces

139

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“…Reduced GSH is the major non-protein thiol in cells and is essential for maintaining the cellular redox status [21]. Because the PTE-induced apoptosis of A549 cells correlated with reactive oxygen species generation, we speculated that PTE treatment might disturb the cellular redox status.…”

Section: Resultsmentioning

confidence: 99%

“…Reduced GSH is the major non-protein thiol in cells and is essential for maintaining the cellular redox status. The intracellular GSH content has a decisive effect on anticancer drug-induced apoptosis, and the apoptotic effects are inversely proportional to the GSH content [21]. The MMP is produced when protons are pumped from the mitochondrial matrix into the inter-membrane space.…”

Section: Discussionmentioning

confidence: 99%

Pterostilbene Exerts Antitumor Activity via the Notch1 Signaling Pathway in Human Lung Adenocarcinoma Cells

et al. 2013

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Although pterostilbene (PTE) has been shown to have potent antitumor activities against various cancer types, the molecular mechanisms of these activities remain unclear. In this study, we investigated the antitumor activity of PTE against human lung adenocarcinoma in vitro and in vivo and explored the role of the Notch1 signaling pathway in this process. PTE treatment resulted in a dose- and time-dependent decrease in the viability of A549 cells. Additionally, PTE exhibited strong antitumor activity, as evidenced not only by a reduced mitochondrial membrane potential (MMP) and a decreased intracellular glutathione content but also by increases in the apoptotic index and the level of reactive oxygen species (ROS). Furthermore, PTE treatment induced the activation of the Notch1 Intracellular Domain (NICD) protein and activated Hes1. DAPT (a gamma secretase inhibitor) and Notch1 siRNA prevented the induction of NICD and Hes1 activation by PTE treatment and sensitized the cells to PTE treatment. The down-regulation of Notch signaling also prevented the activation of pro-survival pathways (most notably the PI3K/Akt pathway) after PTE treatment. In summary, lung adenocarcinoma cells may enhance Notch1 activation as a protective mechanism in response to PTE treatment. Combining a gamma secretase inhibitor with PTE treatment may represent a novel approach for treating lung adenocarcinoma by inhibiting the survival pathways of cancer cells.

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“…HepaRG cells (4.0x10 5 cells/well) were incubated in 6-well plates and treated with different concentrations of emodin (20, 40 and 80 µM) for 24 h at 37˚C. After treatment, the cells were collected and fixed with 70% ice-cold ethanol at 4˚C at least for 24 h, and then stained with PI/RNase A staining buffer solution for 30 min at 37˚C in the dark (36). The resulting suspension was passed through a nylon mesh filter and analyzed by flow cytometry.…”

Section: Analysis Of Mitochondrial Membrane Potential (δψM)mentioning

confidence: 99%

Emodin induces apoptosis in human hepatocellular carcinoma HepaRG cells via the mitochondrial caspase‑dependent pathway

Dong

et al. 2018

Oncol Rep

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Emodin-induced hepatotoxicity in vivo and in vitro has been gaining increasing attention. However, the exact molecular pathways underlying these effects remain poorly clarified. The aim of the present study was to evaluate the cytotoxic effect of emodin on HepaRG cells and to define the underlying mechanism. The results demonstrated that emodin evidently inhibited HepaRG cell growth in a dose- and time-dependent manner by blocking cell cycle progression in the S and G2/M phase and by inducing apoptosis. Emodin treatment also resulted in generation of reactive oxygen species (ROS), which abrogated mitochondrial membrane potential (MMP). The above effects were all suppressed by antioxidants, such as N-acetylcysteine (NAC). Further studies by western blot analysis howed that emodin upregulated p53, p21, Bax, cyclin E, cleaved caspase-3, 8 and 9, and cleaved poly(ADP-ribose)polymerase (PARP). However, the protein expression of Bcl-2, cyclin A and CDK2 was downregulated. Taken together, our results suggest that emodin induces apoptosis via the mitochondrial apoptosis pathway through cell cycle arrest and ROS generation in HepaRG cells.

show abstract

MMPT as a reactive oxygen species generator induces apoptosis via the depletion of intracellular GSH contents in A549 cells

Cited by 21 publications

References 34 publications

Biogenic silver nanoparticles from Abutilon indicum: Their antioxidant, antibacterial and cytotoxic effects in vitro

Biogenic silver nanoparticles from Abutilon indicum: Their antioxidant, antibacterial and cytotoxic effects in vitro

Pterostilbene Exerts Antitumor Activity via the Notch1 Signaling Pathway in Human Lung Adenocarcinoma Cells

Emodin induces apoptosis in human hepatocellular carcinoma HepaRG cells via the mitochondrial caspase‑dependent pathway

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