scholarly journals Oxymatrine promotes hypertrophic scar repair through reduced human scar fibroblast viability, collagen and induced apoptosis via autophagy inhibition

2021 ◽  
Author(s):  
Xingwang Deng ◽  
Fang Zhao ◽  
Dan Zhao ◽  
Qing Zhang ◽  
Yongzhao Zhu ◽  
...  
Keyword(s):  
Hypertrophic Scar ◽  
Induced Apoptosis ◽  
Autophagy Inhibition

scholarly journals Autophagy Inhibition Enhances Daunorubicin-Induced Apoptosis in K562 Cells

PLoS ONE ◽  
2011 ◽  
Vol 6 (12) ◽  
pp. e28491 ◽  
Author(s):  
Weidong Han ◽  
Jie Sun ◽  
Lifeng Feng ◽  
KaiFeng Wang ◽  
Da Li ◽  
...  
Keyword(s):  
K562 Cells ◽  
Induced Apoptosis ◽  
Autophagy Inhibition

scholarly journals Antidepressant Drug Enhanced Trail Receptor-2 Expression and Sensitized Lung Cancer Cells to Trail-Induced Apoptosis via Inhibition of Autophagic Flux

2020 ◽  
Author(s):  
K.M.A. Zinnah ◽  
Jae-Won Seol ◽  
Sang-Youel Park
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Antidepressant Drug ◽  
Lung Cancer Cells ◽  
Autophagic Flux ◽  
Trail Receptor ◽  
Treatment Needs ◽  
Induced Apoptosis ◽  
Autophagy Inhibition

Autophagy, an alternative cell death mechanism, is also termed programmed cell death type II. Autophagy in cancer treatment needs to be regulated. In our study, autophagy inhibition by desipramine or the autophagy inhibitor chloroquine (CQ) enhanced tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor-2 [death receptor (DR5)] expression and subsequently TRAIL-induced apoptosis in TRAIL-resistant A549 lung cancer cells. Genetic inhibition of DR5 substantially reduced desipramine-enhanced TRAIL-mediated apoptosis, proving that DR5 was required to increase TRAIL sensitivity in TRAIL-resistant cancer cells. Desipramine treatment upregulated p62 expression and promoted conversion of light chain 3 (LC3)-I to its lipid-conjugated form, LC3-II, indicating that autophagy inhibition occurred at the final stages of autophagic flux. Transmission electron microscopy analysis showed the presence of condensed autophagosomes, which resulted from the late stages of autophagy inhibition by desipramine. TRAIL, in combination with desipramine or CQ, augmented the expression of apoptosis-related proteins cleaved caspase-8 and cleaved caspase-3. Our results contributed to the understanding of the mechanism underlying the synergistic anti-cancer effect of desipramine and TRAIL and presented a novel mechanism of DR5 upregulation. These findings demonstrated that autophagic flux inhibition by desipramine potentiated TRAIL-induced apoptosis, suggesting that appropriate regulation of autophagy is required for sensitizing TRAIL-resistant cancer cells to TRAIL-mediated apoptosis.

scholarly journals Suppression of Autophagy Sensitizes Osteosarcoma to mTOR Inhibition

2020 ◽  
Author(s):  
Ke Zeng ◽  
Lei Jin ◽  
Xiao Yang ◽  
Zhengjie Yang ◽  
Guoxin Zhu
Keyword(s):  
Combination Therapy ◽  
Colony Formation ◽  
Resistance Mechanism ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Mtor Inhibition ◽  
Major Health Problem ◽  
Induced Apoptosis ◽  
Autophagy Inhibition

Abstract Aim Osteosarcoma is some major health problem. We intended to investigate the role of Rapamycin and autophagy inhibition in the treatment of osteosarcoma. Method We conducted a series of in vitro studies using two osteosarcoma cell lines. Using genetic and pharmaceutical interventions we studied whether combined autophagy inhibition could sensitize osteosarcoma sales to a Rapamycin treatment. Proliferation, innovation, migration, and colony formation assays were performed. Results Osteosarcoma cells had low basal autophagy levels. Inhibition of mTOR only demonstrated moderate effects but induced increased autophagy levels, indicating possible resistance mechanism. Inhibition of both autophagy and mTOR axis synergistically inhibited proliferation, migration, invasion, and colony formation of osteosarcoma cells. The combination therapy induced apoptosis, which could be restored in part by NEC1. Conclusion Increased autophagy level was responsible for compromised effect of mTOR inhibition in osteosarcoma. Combination therapy using rapamycin and chloroquine held promise to the development of novel mortality.

scholarly journals Autophagy inhibition enhances celecoxib-induced apoptosis in osteosarcoma

Cell Cycle ◽  
2018 ◽  
Vol 17 (8) ◽  
pp. 997-1006 ◽  
Author(s):  
Pingting Zhou ◽  
Yanyan Li ◽  
Bo Li ◽  
Meichao Zhang ◽  
Ci Xu ◽  
...  
Keyword(s):  
Induced Apoptosis ◽  
Autophagy Inhibition

Autophagy Inhibition Promotes Quercetin Induced Apoptosis in MG-63 Human Osteosarcoma cells

2015 ◽  
Vol 40 (2) ◽  
pp. 85-91 ◽  
Author(s):  
Sung-Jin Park ◽  
◽  
Su-Bin Yu ◽  
Yong-Ho Kim ◽  
In-Ryoung Kim ◽  
...  
Keyword(s):  
Osteosarcoma Cells ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells ◽  
Induced Apoptosis ◽  
Autophagy Inhibition

Autophagy inhibition potentiates ruxolitinib-induced apoptosis in JAK2V617F cells

2019 ◽  
Vol 38 (3) ◽  
pp. 733-745
Author(s):  
João Agostinho Machado-Neto ◽  
Juan Luiz Coelho-Silva ◽  
Fábio Pires de Souza Santos ◽  
Priscila Santos Scheucher ◽  
Paulo Vidal Campregher ◽  
...  
Keyword(s):  
Induced Apoptosis ◽  
Autophagy Inhibition

scholarly journals Autophagy Inhibition Enhances Apoptosis Induced by Dioscin in Huh7 Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Ming-Ju Hsieh ◽  
Shun-Fa Yang ◽  
Yih-Shou Hsieh ◽  
Tzy-Yen Chen ◽  
Hui-Ling Chiou
Keyword(s):  
Cell Apoptosis ◽  
Caspase 3 ◽  
Natural Food ◽  
Dependent Manner ◽  
Caspase Activation ◽  
Huh7 Cells ◽  
Dependent Cell ◽  
Induced Apoptosis ◽  
Dose Dependent ◽  
Autophagy Inhibition

Extensive research results support the application of herbal medicine or natural food as an augment during therapy for various cancers. However, the effect of dioscin on tumor cells autophagy has not been clearly clarified. In this study, the unique effects of dioscin on autophagy of hepatoma cells were investigated. Results found that dioscin induced caspase-3- and -9-dependent cell apoptosis in a dose-dependent manner. Moreover, inhibition of ERK1/2 phosphorylation significantly abolished the dioscin-induced apoptosis. In addition, dioscin triggered cell autophagy in early stages. With autophagy inhibitors to hinder the autophagy process, dioscin-induced cell apoptosis was significantly enhanced. An inhibition of caspase activation did not affect the dioscin-induced LC3-II protein expression. Based on the results, we believed that while apoptosis was blocked, dioscin-induced autophagy process also diminished in Huh7 cells. In conclusion, this study indicates that dioscin causes autophagy in Huh7 cells and suggests that dioscin has a cytoprotective effect.

Inactivation of Beclin-1-dependent autophagy promotes ursolic acid-induced apoptosis in hypertrophic scar fibroblasts

2017 ◽  
Vol 27 (1) ◽  
pp. 58-63 ◽  
Author(s):  
Chuan Cao ◽  
Wenping Wang ◽  
Lele Lu ◽  
Liang Wang ◽  
XiaoSong Chen ◽  
...  
Keyword(s):  
Ursolic Acid ◽  
Hypertrophic Scar ◽  
Beclin 1 ◽  
Induced Apoptosis
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