Dihydroartemisinin induces apoptosis in human bladder cancer cell lines through reactive oxygen species, mitochondrial membrane potential, and cytochrome C pathway

Poupel, Farhad; Aghaei, Mahmoud; Ahmad, Mansoor; Jafari, Seyyed Mehdi; Shahrestanaki, Mohammad Keyvanloo

doi:10.4103/ijpvm.ijpvm_258_17

Cited by 20 publications

(8 citation statements)

References 36 publications

(52 reference statements)

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“…The maintenance of the mitochondrial membrane potential (Δψm) is crucial for mitochondrial function. The collapse of ΔΨm and depletion of ATP are the direct consequences of ROS accumulation in mitochondria, and these events precede the release of cytochrome c and activation of the caspase protease cascade [ 38 ]. We have found that AGEs induce a significant depletion in the ΔΨm of GMCs, a result that is in agreement with those reported in previous studies [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Kaempferitrin on Advanced Glycation End Products Induce Mesangial Cell Apoptosis and Oxidative Stress

Jiang

Wang

Liu

et al. 2018

IJMS

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Advanced glycation end products (AGEs) and the receptor for AGEs (RAGE) both play important roles in diabetic nephropathy (DN). Previous studies have identified glomerular mesangial cells (GMCs) injury as a key early risk factor in the development of DN. Kaempferitrin (KM) is a potent antioxidant with hypoglycemic action. Although KM is known to protect against AGE-induced damage in GMCs, the effects and the mechanisms by which they occur are poorly understood. In this study, cultured rat GMCs were exposed to AGE-induced oxidative stress (OS) to model DN in vitro. Reactive oxygen species (ROS) was analyzed by 2′,7′-dichlorofluorescin diacetate (DCFH-DA). Superoxide dismutase (SOD) and malondialdehyde (MDA) were studied using commercial kits. Mitochondrial membrane potential (Δψm) was measured by rhodamine 123. Hoechst 33258 and annexin V and propidium iodide (PI) double staining were performed to observe the apoptosis states in GMCs, whereas apoptosis and protective mechanism in AGE-induced GMCs were investigated by Western blot. The data revealed that KM effectively increased SOD activity, decreased MDA levels, suppressed ROS generation, and protected against OS in AGE-induced GMCs. Treatment with KM also inhibited the expression of collagen IV and transforming growth factor-β1 (TGF-β1), improved mitochondrial membrane potential recovery, and suppressed the mitochondrial/cytochrome c-mediated apoptosis pathway through the expression of anti-apoptotic factors in GMCs in vitro. These findings suggest that KM may be a new potential agent in the treatment of DN in future.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Kaempferitrin on Advanced Glycation End Products Induce Mesangial Cell Apoptosis and Oxidative Stress

Jiang

Wang

Liu

et al. 2018

IJMS

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“…6B ). The decrease of MMP has been associated with the increase of ROS, and with cell apoptosis ( 11 , 27 ).…”

Section: Resultsmentioning

confidence: 99%

Pancreatic cancer cell apoptosis is induced by a proteoglycan extracted from Ganoderma lucidum

Jiang

Zeng

et al. 2020

Oncol Lett

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The Traditional Chinese Medicine, Ganoderma lucidum , has been widely used for its immunity-related and anti-cancer effects. Fudan-Yueyang-Ganoderma lucidum (FYGL) is a proteoglycan, extracted from Ganoderma lucidum , that has shown safe anti-diabetic activity in vivo . The present study demonstrated that FYGL could selectively inhibit the viability of PANC-1 and BxPC-3 pancreatic cancer cells in a dose dependent manner, but not in Mia PaCa-2 pancreatic cancer cells and HepG2 liver cancer cells. In addition, FYGL could inhibit migration and colony formation, and promote apoptosis in PANC-1 cells, but not in Mia PaCa-2 cells. Further investigation into the underlying mechanism revealed that FYGL could inhibit the expression level of the Bcl-2 protein in PANC-1 cells, but not in Mia PaCa-2 cells, leading to an increase in reactive oxygen species (ROS) and a reduction in the mitochondrial membrane potential and cell apoptosis. The increased ROS also promoted the formation of autophagosomes, along with an increase in the microtubule-associated protein light chain 3 II/I ratio. However, FYGL halted autophagy by preventing the autophagosomes from entering the lysosomes. The inhibition of autophagy increased the accumulation of defective mitochondria, as well as the production of ROS. Taken together, the processes of ROS regulation and autophagy inhibition promoted apoptosis of PANC-1 cells through the caspase-3/cleaved caspase-3 cascade. These results indicated that FYGL could be potentially used as an anti-cancer agent in the treatment of pancreatic cancer.

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“…The Bax and Bcl2 protein were determined by immunoblotting assays as described previously(2122). The cells were treated with different concentrations of Gal-9 (1, 50, and 100 nM) for 48 h. Prepared lysates at 30-50 μg amounts were subjected to SDS-PAGE and transferred onto polyvinylidene difluoride (PVDF) membrane.…”

Section: Methodsmentioning

confidence: 99%

Galectin-9 induces apoptosis in OVCAR-3 ovarian cancer cell through mitochondrial pathway

et al. 2018

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Galectin-9 (Gal-9), a member of animal lectins' family, is implicated in the induction of apoptosis in various cancer cells. Here, we evaluated the anti-tumor effect of Gal-9 in OVCAR-3 ovarian cancer cells. The effect of the Gal-9 on cell viability was evaluated using MTT assays. Apoptosis was assessed using Annexin-V staining. The assessment of mitochondrial membrane potential (ΔΨm) was performed using a JC-1 probe. The activity of caspase-3 and caspase-6 were evaluated with colorimetric assay. The production of reactive oxygen species (ROS) was applied by fluorescent probe. The expression levels of Bax and Bcl-2 were assessed using western blotting. The result showed that Gal-9 inhibits cell viability. Flow cytometry analysis showed that Gal-9 induces apoptosis in ovarian cancer cells. Moreover, Gal-9 decreased ΔΨm and increased the generation of ROS and caspase-3 and caspase-6 activities in ovarian cancer cells. Moreover, Gal-9 induced expression of Bax as well as inhibited expression of Bcl-2. In conclusion, our results indicated that Gal-9 induced apoptosis in ovarian cancer cells through mitochondrial pathway.

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Dihydroartemisinin induces apoptosis in human bladder cancer cell lines through reactive oxygen species, mitochondrial membrane potential, and cytochrome C pathway

Cited by 20 publications

References 36 publications

Protective Effects of Kaempferitrin on Advanced Glycation End Products Induce Mesangial Cell Apoptosis and Oxidative Stress

Protective Effects of Kaempferitrin on Advanced Glycation End Products Induce Mesangial Cell Apoptosis and Oxidative Stress

Pancreatic cancer cell apoptosis is induced by a proteoglycan extracted from Ganoderma lucidum

Galectin-9 induces apoptosis in OVCAR-3 ovarian cancer cell through mitochondrial pathway

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