A Benzylideneacetophenone Derivative Induces Apoptosis of Radiation-Resistant Human Breast Cancer Cells via Oxidative Stress

Park, Jeong Eon; Piao, Mei Jing; Kang, Kyoung Ah; Shilnikova, Kristina; Hyun, Yu Jae; Oh, Sei Kwan; Jeong, Young Jin; Chae, Sungwook; Hyun, Jin Won

doi:10.4062/biomolther.2017.010

Cited by 10 publications

(11 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cell-coated slides were immersed in lysis buffer (2.5 M NaCl, 100 mM Na-EDTA, 10 mM Tris, 1% Trion X-100, and 10% DMSO, pH 10) for 1 h at 4 °C, subjected to electrophoresis, stained with ethidium bromide, and observed under a fluorescence microscope equipped with an image analysis software (Kinetic Imaging, Komet 5.5, UK) as previously described (Park et al 2017 ). The percentage of the total fluorescence in the comet tail and the length of the tail was recorded in 50 cells per slide.…”

Section: Methodsmentioning

confidence: 99%

Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis

et al. 2018

Self Cite

View full text Add to dashboard Cite

The skin is the largest organ of the human body and the one mostly exposed to outdoor contaminants. To evaluate the biological mechanisms underlying skin damage caused by fine particulate matter (PM2.5), we analyzed the effects of PM2.5 on cultured human keratinocytes and the skin of experimental animals. PM2.5 was applied to human HaCaT keratinocytes at 50 µg/mL for 24 h and to mouse skin at 100 µg/mL for 7 days. The results indicate that PM2.5 induced oxidative stress by generating reactive oxygen species both in vitro and in vivo, which led to DNA damage, lipid peroxidation, and protein carbonylation. As a result, PM2.5 induced endoplasmic reticulum stress, mitochondrial swelling, and autophagy, and caused apoptosis in HaCaT cells and mouse skin tissue. The PM2.5-induced cell damage was attenuated by antioxidant N-acetyl cysteine, confirming that PM2.5 cellular toxicity was due to oxidative stress. These findings contribute to understanding of the pathophysiological mechanisms triggered in the skin by PM2.5, among which oxidative stress may play a major role.

show abstract

Section: Methodsmentioning

confidence: 99%

Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis

et al. 2018

Self Cite

View full text Add to dashboard Cite

show abstract

“…Hoechst 33342 (1 μg/ml) was added to each well and the cells were further incubated at 37°C for 30 min in the dark. Control and apoptotic SH-SY5Y cells were visualized under a fluorescence microscope equipped with a CoolSNAP-Pro color digital camera to examine the degree of nuclear condensation (Park et al ., 2017).…”

Section: Methodsmentioning

confidence: 99%

7,8-Dihydroxyflavone Protects High Glucose-Damaged Neuronal Cells against Oxidative Stress

Cho

Kang

Piao

et al. 2019

Biomolecules & Therapeutics

Self Cite

View full text Add to dashboard Cite

Oxidative stress is considered a major contributor in the pathogenesis of diabetic neuropathy and in diabetes complications, such as nephropathy and cardiovascular diseases. Diabetic neuropathy, which is the most frequent complications of diabetes, affect sensory, motor, and autonomic nerves. This study aimed to investigate whether 7,8-dihydroxyflavone (7,8-DHF) protects SH-SY5Y neuronal cells against high glucose-induced toxicity. In the current study, we found that diabetic patients exhibited higher lipid peroxidation caused by oxidative stress than healthy subjects. 7,8-DHF exhibits superoxide anion and hydroxyl radical scavenging activities. High glucose-induced toxicity severely damaged SH-SY5Y neuronal cells, causing mitochondrial depolarization; however, 7,8-DHF recovered mitochondrial polarization. Furthermore, 7,8-DHF effectively modulated the expression of pro-apoptotic protein (Bax) and anti-apoptotic protein (Bcl-2) under high glucose, thus inhibiting the activation of caspase signaling pathways. These results indicate that 7,8-DHF has antioxidant effects and protects cells from apoptotic cell death induced by high glucose. Thus, 7,8-DHF may be developed into a promising candidate for the treatment of diabetic neuropathy.

show abstract

“…Several reports have shown that the increase in citrate intracellular levels inhibits proliferation, induces apoptosis in cancer cells of different origin, and reduces tumor growth of several xenografts in mice synergizing with anti-cancer treatment [17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33]. The majority of studies investigating the anti-cancer role of citrate describe the inhibitory effect of acute citrate administration, and, according to the literature, the fate of cells surviving citrate treatment has not been investigated yet.…”

Section: Introductionmentioning

confidence: 99%

Effects of Long-Term Citrate Treatment in the PC3 Prostate Cancer Cell Line

Caiazza

D’Agostino

Passaro

et al. 2019

IJMS

View full text Add to dashboard Cite

Acute administration of a high level of extracellular citrate displays an anti-proliferative effect on both in vitro and in vivo models. However, the long-term effect of citrate treatment has not been investigated yet. Here, we address this question in PC3 cells, a prostate-cancer-derived cell line. Acute administration of high levels of extracellular citrate impaired cell adhesion and inhibited the proliferation of PC3 cells, but surviving cells adapted to grow in the chronic presence of 20 mM citrate. Citrate-resistant PC3 cells are significantly less glycolytic than control cells. Moreover, they overexpress short-form, citrate-insensitive phosphofructokinase 1 (PFK1) together with full-length PFK1. In addition, they show traits of mesenchymal-epithelial transition: an increase in E-cadherin and a decrease in vimentin. In comparison with PC3 cells, citrate-resistant cells display morphological changes that involve both microtubule and microfilament organization. This was accompanied by changes in homeostasis and the organization of intracellular organelles. Thus, the mitochondrial network appears fragmented, the Golgi complex is scattered, and the lysosomal compartment is enlarged. Interestingly, citrate-resistant cells produce less total ROS but accumulate more mitochondrial ROS than control cells. Consistently, in citrate-resistant cells, the autophagic pathway is upregulated, possibly sustaining their survival. In conclusion, chronic administration of citrate might select resistant cells, which could jeopardize the benefits of citrate anticancer treatment.

show abstract

A Benzylideneacetophenone Derivative Induces Apoptosis of Radiation-Resistant Human Breast Cancer Cells via Oxidative Stress

Cited by 10 publications

References 27 publications

Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis

Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis

7,8-Dihydroxyflavone Protects High Glucose-Damaged Neuronal Cells against Oxidative Stress

Effects of Long-Term Citrate Treatment in the PC3 Prostate Cancer Cell Line

Contact Info

Product

Resources

About