Andrographolide sensitizes cancer cells to TRAIL-induced apoptosis via p53-mediated death receptor 4 up-regulation

Zhou, Jing; Lu, Guo‐Dong; Ong, Chye-Sun; Ong, Choon‐Nam; Shen, Han‐Ming

doi:10.1158/1535-7163.mct-08-0071

Cited by 106 publications

(84 citation statements)

References 52 publications

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“…in rats and found that the blood concentration of andrographolide was approximately 11 mg/mL ($30 mM). At this concentration, andrographolide was reported to possess anti-inflammatory, anti-tumor and anti-thrombotic properties in in vitro studies (Bao et al, 2009;Lu et al, 2011Lu et al, , 2012Zhou et al, 2008). In the present study, our data showed that andrographolide at 50 mM caused CEC death or apoptosis (Figures 1 and 2).…”

Section: Discussionsupporting

confidence: 62%

A novel bioactivity of andrographolide fromAndrographis paniculataon cerebral ischemia/reperfusion-induced brain injury through induction of cerebral endothelial cell apoptosis

Yen

Hsu

Huang

et al. 2013

Pharmaceutical Biology

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Context: Andrographolide, extracted from the leaves of Andrographis paniculata (Burm. f.) Nees (Acanthaceae), is a labdane diterpene lactone. It is widely reported to possess antiinflammatory and antitumorigenic activities. Cerebral endothelial cells (CECs) play a crucial role in supporting the integrity and the function of the blood-brain barrier (BBB). However, no data are available concerning the effects of andrographolide in CECs. The aim of this study was to examine the detailed mechanisms of andrographolide on CECs.Objective: This study investigated a novel bioactivity of andrographolide on cerebral ischemia/ reperfusion-induced brain injury. Materials and methods: CECs were treated with andrographolide (20-100 mL) for the indicated times (0-24 h). After the reactions, cell survival rate and cytotoxicity were tested by the MTT assay and the lactate dehydrogenase (LDH) test, respectively. Western blotting was used to detect caspase-3 expression. In addition, analysis of cell cycle and apoptosis using PI staining and annexin V-FITC/PI labeling, respectively, was performed by flow cytometry. We also investigated the effect of andrographolide on middle cerebral artery occlusion (MCAO)/reperfusion-induced brain injury in a rat model. Results: In the present study, we found that andrographolide (50-100 mL) markedly inhibited CEC growth according to an MTT assay and caused CEC damage according to a LDH test. Our data also revealed that andrographolide (50 mM) induced CEC apoptosis and caspase-3 activation as respectively detected by PI/annexin-V double staining and western blotting. Moreover, andrographolide arrested the CEC cell cycle at the G0/G1 phase by PI staining. In addition, andrographolide (5 mg/kg) caused deterioration of MCAO/reperfusion-induced brain injury in a rat model. Conclusions: These data suggest that andrographolide may disrupt BBB integrity, thereby deteriorating MCAO/reperfusion-induced brain injury, which are, in part, associated with its capacity to arrest cell-cycle and induce CEC apoptosis.

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Section: Discussionsupporting

confidence: 62%

A novel bioactivity of andrographolide fromAndrographis paniculataon cerebral ischemia/reperfusion-induced brain injury through induction of cerebral endothelial cell apoptosis

Yen

Hsu

Huang

et al. 2013

Pharmaceutical Biology

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“…Numerous natural compounds such as triptolide (isolated from the Chinese herb Tripterygium wilfordii Hook), alpha-tocopheryl succinate (a-TOS, an analogue of vitamin E), and andrographolide (a diterpenoid lactone isolated from a traditional herbal medicine Andrographis paniculata) upregulate the expression of DRs directly through the induction of p53. [134][135][136] It has also been reported that ROS participates in the induction of DRs by 6-dehydrogingerdione (a compound isolated from the rhizomes of Zingiber officinale) mediated through expression of p53. 137 However, nimbolide, azadirone, and g-yocotrienol induce DR expression through p53 expression that is mediated by an ERK-p53 mechanism(s).…”

Section: Natural Compounds That Can Sensitize Tumor Cells To Trailmentioning

confidence: 99%

Targeting TNF-related apoptosis-inducing ligand (TRAIL) receptor by natural products as a potential therapeutic approach for cancer therapy

Dai

Zhang

Arfuso

et al. 2015

Exp Biol Med (Maywood)

165

109

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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to selectively induce apoptotic cell death in various tumor cells by engaging its death-inducing receptors (TRAIL-R1 and TRAIL-R2). This property has led to the development of a number of TRAIL-receptor agonists such as the soluble recombinant TRAIL and agonistic antibodies, which have shown promising anticancer activity in preclinical studies. However, besides activating caspase-dependent apoptosis in several cancer cells, TRAIL may also activate nonapoptotic signal transduction pathways such as nuclear factor-kappa B, mitogen-activated protein kinases, AKT, and signal transducers and activators of transcription 3, which may contribute to TRAIL resistance that is being now frequently encountered in various cancers. TRAIL resistance can be overcome by the application of efficient TRAILsensitizing pharmacological agents. Natural compounds have shown a great potential in sensitizing cells to TRAIL treatment through suppression of distinct survival pathways. In this review, we have summarized both apoptotic and nonapoptotic pathways activated by TRAIL, as well as recent advances in developing TRAIL-receptor agonists for cancer therapy. We also briefly discuss combination therapies that have shown great potential in overcoming TRAIL resistance in various tumors.

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“…1 Both authors contributed equally to this work. 2 ptosis (11). Andrographolide was also shown to interfere with T-cell activation and dendritic cell maturation (12).…”

Section: Recent Studies Have Demonstrated That Transcription Factor Nmentioning

confidence: 99%

Andrographolide Enhances Nuclear Factor-κB Subunit p65 Ser536 Dephosphorylation through Activation of Protein Phosphatase 2A in Vascular Smooth Muscle Cells

Hsieh

Hsu

Hsiao

et al. 2011

Journal of Biological Chemistry

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Recent studies have demonstrated that transcription factor nuclear factor (NF)-B inhibition may contribute to the protective anti-inflammatory actions of andrographolide, an abundant component of plants of the genus Andrographis. However, the precise mechanism by which andrographolide inhibits NF-B signaling remains unclear. We thus investigated the mechanism involved in andrographolide suppression of NF-B signaling in rat vascular smooth muscle cells (VSMCs) exposed to proinflammatory stimuli, LPS, and IFN-␥. Andrographolide was shown to suppress LPS/IFN-␥-induced inducible nitric-oxide synthase and matrix metalloprotease 9 expression in rat VSMCs. Andrographolide also inhibited LPS/IFN-␥-induced p65 nuclear translocation, DNA binding activity, p65 Ser 536 phosphorylation, and NF-B reporter activity. However, IKK phosphorylation and downstream inhibitory B␣ phosphorylation and degradation were not altered by the presence of andrographolide in LPS/IFN-␥-stimulated VSMCs. These andrographolide inhibitory actions could be prevented by selective inhibition of neutral sphingomyelinase and protein phosphatase 2A (PP2A). Furthermore, andrographolide was demonstrated to increase ceramide formation and PP2A activity in VSMCs and to inhibit neointimal formation in rat carotid injury models. These results suggest that andrographolide caused neutral sphingomyelinase-mediated ceramide formation and PP2A activation to dephosphorylate p65 Ser 536 , leading to NF-B inactivation and subsequent inducible nitric-oxide synthase down-regulation in rat VSMCs stimulated by LPS and IFN-␥.

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Andrographolide sensitizes cancer cells to TRAIL-induced apoptosis via p53-mediated death receptor 4 up-regulation

Abstract: Tumor necrosis factor-related apoptosis-inducing ligand

Cited by 106 publications

References 52 publications

A novel bioactivity of andrographolide fromAndrographis paniculataon cerebral ischemia/reperfusion-induced brain injury through induction of cerebral endothelial cell apoptosis

A novel bioactivity of andrographolide fromAndrographis paniculataon cerebral ischemia/reperfusion-induced brain injury through induction of cerebral endothelial cell apoptosis

Targeting TNF-related apoptosis-inducing ligand (TRAIL) receptor by natural products as a potential therapeutic approach for cancer therapy

Andrographolide Enhances Nuclear Factor-κB Subunit p65 Ser536 Dephosphorylation through Activation of Protein Phosphatase 2A in Vascular Smooth Muscle Cells

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