Dracorhodin perchlorate induces G1/G0 phase arrest and mitochondria-mediated apoptosis in SK-MES-1 human lung squamous carcinoma cells

Zhang, Guangxin; Sun, Mei; Zhang, Yifan; Hua, Peiyan; Li, Xin; Cui, Ranji; Zhang, Xingyi

doi:10.3892/ol.2015.3212

Cited by 9 publications

(13 citation statements)

References 39 publications

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“…Thus, more detailed research is needed about the protective effect of DP against apoptosis in INS-1cells exposed in vitro to glucotoxicity or lipotoxicity. It is noteworthy that some studies have showed a pro-apoptotic role of DP in cancer cells [12,13], which seems contradictory to its anti-apoptotic effects observed in the present study. However, we noticed that the concentrations of DP used to induce apoptosis in multiple types of cells lines [32,33], were generally higher than the concentration of DP (20 lgÁmL À1 ) in our experiment.…”

Section: Discussioncontrasting

confidence: 99%

“…MAPK-dependent signaling pathways are known to be involved in b-cell dysfunction. It is noteworthy that some studies have showed a pro-apoptotic role of DP in cancer cells [12,13], which seems contradictory to its anti-apoptotic effects observed in the present study. Moreover, Pdx1 is a target of insulin, which exerts its anti-apoptotic effect through insulin signaling.…”

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confidence: 99%

“…Although dracorhodin has already been reported to have various pharmacological activities, including antimicrobial and antiviral roles, it is not stable in solution. DP is one main derivative of dracorhodin that has been shown to have cytotoxic effects, mainly by inducing apoptosis, on a variety of tumor cells, such as human prostate cancer cells, human lung squamous carcinoma cells, human breast cancer cells, human premyelocytic leukemia cells, melanoma cells and glioma cells [12,13]. Also, the effect of DP and its mechanism of preventing renal injury in early diabetic nephropathy were determined in 2008 [14].…”

Section: Introductionmentioning

confidence: 99%

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Dracorhodin perchlorate protects pancreatic β‐cells against glucotoxicity‐ or lipotoxicity‐induced dysfunction and apoptosis in vitro and in vivo

et al. 2019

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Glucotoxicity or lipotoxicity leads to hyperglycemia and insulin secretion deficiency, which are important causes for the onset of type 2 diabetes mellitus (T2DM). Thus, the restoration of β‐cell function is a long‐sought goal in diabetes research. Previous studies have implicated pancreatic and duodenal homeobox 1 gene (Pdx1) in β‐cell function and insulin secretion. In this study, we established a Pdx1 promoter‐dependent luciferase system and identified the natural compound dracorhodin perchlorate (DP) as an effective promotor of Pdx1 expression. We further demonstrated that DP could significantly inhibit β‐cell apoptosis induced by 33 mm glucose or 200 μm palmitate by interfering with endoplasmic reticulum stress and mitochondrial pathways and enhance insulin secretion as well. These effects were associated with enhanced activities of Erk1/2, which in turn promoted Pdx1 expression and increased the ratio of Bcl2/Bax, since inhibition of the Erk1/2 pathway abolished the DP‐induced expression of Pdx1 and suppression of apoptosis. In addition, our in vivo results in diabetic mice indicated that DP treatment lowered blood glucose, raised insulin levels, enhanced Pdx1 expression and increased islet size and number in the pancreas of diabetic mice. Our findings suggest that Pdx1 is a potential target molecule of DP in the treatment of T2DM via the inhibition of glucotoxicity‐ or lipotoxicity‐ induced β‐cell apoptosis and the attenuation of insulin secretion dysfunction.

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Section: Discussioncontrasting

confidence: 99%

contrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Dracorhodin perchlorate protects pancreatic β‐cells against glucotoxicity‐ or lipotoxicity‐induced dysfunction and apoptosis in vitro and in vivo

et al. 2019

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“…6,7 D.P is found to have an anti-cancer function by inducing apoptosis in human cancer cells. [8][9][10][11][12] Reported in some other literatures, D.P has anti-microbial effects by reducing the production of α-toxin by Staphylococcus aureus 13 and inhibiting the formation of biofilm and virulence factors of Candida albicans. 14 We have confirmed that several compounds extracted from S draxonis resin have inhibitory effects on osteoclast differentiation.…”

Section: Introductionmentioning

confidence: 98%

“…D.P also exerts strong angiogenic effects, which can be beneficial for wound healing . D.P is found to have an anti‐cancer function by inducing apoptosis in human cancer cells . Reported in some other literatures, D.P has anti‐microbial effects by reducing the production of α‐toxin by Staphylococcus aureus and inhibiting the formation of biofilm and virulence factors of Candida albicans .…”

Section: Introductionmentioning

confidence: 99%

Dracorhodin perchlorate inhibits osteoclastogenesis through repressing RANKL‐stimulated NFATc1 activity

Wang

et al. 2020

J Cellular Molecular Medi

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Osteolytic skeletal disorders are caused by an imbalance in the osteoclast and osteoblast function. Suppressing the differentiation and resorptive function of osteoclast is a key strategy for treating osteolytic diseases. Dracorhodin perchlorate (D.P), an active component from dragon blood resin, has been used for facilitating wound healing and anti‐cancer treatments. In this study, we determined the effect of D.P on osteoclast differentiation and function. We have found that D.P inhibited RANKL‐induced osteoclast formation and resorbed pits of hydroxyapatite‐coated plate in a dose‐dependent manner. D.P also disrupted the formation of intact actin‐rich podosome structures in mature osteoclasts and inhibited osteoclast‐specific gene and protein expressions. Further, D.P was able to suppress RANKL‐activated JNK, NF‐κB and Ca2+ signalling pathways and reduces the expression level of NFATc1 as well as the nucleus translocation of NFATc1. Overall, these results indicated a potential therapeutic effect of D.P on osteoclast‐related conditions.

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Costunolide Induces Apoptosis through Generation of ROS and Activation of P53 in Human Esophageal Cancer Eca-109 Cells

Hua

Sun

Zhang

et al. 2016

J Biochem Mol Toxicol

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Costunolide is a sesquiterpene lactone, which possesses potent anti-cancer properties. However, there is little report about its effects on esophageal cancer. In our study, we investigated the effects of costunolide on the cell viability, cell cycle, and apoptosis in human esophageal cancer Eca-109 cells. It was found that costunolide inhibited the growth of Eca-109 cells in a dose-dependent manner, which was associated with the loss of mitochondrial membrane potential (Δψm ) and the production of ROS. Costunolide induced apoptosis of Eca-109 cells as well as cell cycle arrest in G1/S phase by upregulation of P53 and P21. Costunolide triggered apoptosis in esophageal cancer cells via the upregulation of Bax, downregulation of Bcl-2, and significant activation of caspase-3 and poly ADP-ribose polymerase. These effects were markedly abrogated when cells were pretreated with N-acetylcysteine, a specific reactive oxygen specie inhibitor. These results suggest that costunolide is a potential candidate for the treatment of esophageal cancer.

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Dracorhodin perchlorate induces G1/G0 phase arrest and mitochondria-mediated apoptosis in SK-MES-1 human lung squamous carcinoma cells

Cited by 9 publications

References 39 publications

Dracorhodin perchlorate protects pancreatic β‐cells against glucotoxicity‐ or lipotoxicity‐induced dysfunction and apoptosis in vitro and in vivo

Dracorhodin perchlorate protects pancreatic β‐cells against glucotoxicity‐ or lipotoxicity‐induced dysfunction and apoptosis in vitro and in vivo

Dracorhodin perchlorate inhibits osteoclastogenesis through repressing RANKL‐stimulated NFATc1 activity

Costunolide Induces Apoptosis through Generation of ROS and Activation of P53 in Human Esophageal Cancer Eca-109 Cells

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