14-Deoxy-11,12-didehydroandrographolide induces DDIT3-dependent endoplasmic reticulum stress-mediated autophagy in T-47D breast carcinoma cells

Tan, Heng Kean; Muhammad, Tengku Sifzizul Tengku; Tan, Mei Lan

doi:10.1016/j.taap.2016.03.017

Cited by 19 publications

(16 citation statements)

References 63 publications

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“…To determine the siDDIT3 silencing effects in T-47D cells, the mRNA and protein expression of DDIT3 were evaluated in siDDIT3-transfected cells. Briefly, cells were first transfected with 30 nM of ON-TARGETplus™ SMARTpool DDIT3 siRNA (siDDIT3) or ON-TARGETplus™ Non-targeting Pool siRNA (siControl) (Dharmacon, USA) using Lipofectamine® RNAiMAX Reagent (Invitrogen, USA) for 72 h. Total RNA was then isolated as described previously [1] . Primers for DDIT3 were designed using Beacon Designer 7.80 (Premier Biosoft International, USA).…”

Section: Experimental Design Materials and Methodsmentioning

confidence: 99%

“…Total cellular protein was isolated using ProteoJET™ Mammalian Cell Lysis Reagent (Fermentas, Canada) as described previously [1] . Briefly, the proteins were first separated by SDS-PAGE and then transferred to PVDF membrane.…”

Section: Experimental Design Materials and Methodsmentioning

confidence: 99%

“… The data presented in this article are related to the research article entitled “14-deoxy-11,12-didehydroandrographolide induces DDIT3-dependent endoplasmic reticulum stress-mediated autophagy in T-47D breast carcinoma cells”, which the mechanistic toxicology properties of 14-deoxy-11,12-didehydroandrographolide (14-DDA) were investigated (Tan et al, 2016 [1] ). This article describes the derivation of cytotoxic parameters of 14-DDA, cell viability data after double transfection and DDIT3 silencing in T-47D cells.…”

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confidence: 99%

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Cytotoxic data of 14-deoxy-11, 12-didehydroandrographolide (14-DDA), double transfection and DDIT3 silencing data in T-47D breast carcinoma cells

2016

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The data presented in this article are related to the research article entitled “14-deoxy-11,12-didehydroandrographolide induces DDIT3-dependent endoplasmic reticulum stress-mediated autophagy in T-47D breast carcinoma cells”, which the mechanistic toxicology properties of 14-deoxy-11,12-didehydroandrographolide (14-DDA) were investigated (Tan et al., 2016 [1]). This article describes the derivation of cytotoxic parameters of 14-DDA, cell viability data after double transfection and DDIT3 silencing in T-47D cells.

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Section: Experimental Design Materials and Methodsmentioning

confidence: 99%

Section: Experimental Design Materials and Methodsmentioning

confidence: 99%

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confidence: 99%

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Cytotoxic data of 14-deoxy-11, 12-didehydroandrographolide (14-DDA), double transfection and DDIT3 silencing data in T-47D breast carcinoma cells

2016

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“…When autophagy was induced by leucine starvation in MEFs, a range of core autophagy genes and cytosolic cargo receptors were identified as PERK-dependent ATF4 transcriptional targets, including Map1lc3b, Atg5, Atg3, Atg7, Atg10, Atg12, Atg16l1, Becn1, Gabarap, Gabarapl2, p62 and Nbr1 [ 52 ]. Other pharmacologic ER stressors inducing general autophagic flux include A23187, thapsigargin, tunicamycin, brefeldin A (HCT116 human colon and DU145 human prostate carcinoma cells, and MEFs), cocaine (A172 human astrocytoma cells) and 14-deoxy-11,12-didehydroandrographolide (T47D human breast carcinoma cells) [ 53 – 55 ]. The selectivity of autophagy was addressed in HCT116 and DU145 cells via ultrastructural characterization of autophagosomes, which were shown to contain a variety of cargo, suggesting a general up-regulation of relatively non-selective autophagy [ 53 ].…”

Section: Autophagy and Its Role In Er Homeostasismentioning

confidence: 99%

ER homeostasis and autophagy

Smith

Wilkinson

2017

Essays in Biochemistry

176

126

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The endoplasmic reticulum (ER) is a key site for lipid biosynthesis and folding of nascent transmembrane and secretory proteins. These processes are maintained by careful homeostatic control of the environment within the ER lumen. Signalling sensors within the ER detect perturbations within the lumen (ER stress) and employ downstream signalling cascades that engage effector mechanisms to restore homeostasis. The most studied signalling mechanism that the ER employs is the unfolded protein response (UPR), which is known to increase a number of effector mechanisms, including autophagy. In this chapter, we will discuss the emerging role of autophagy as a UPR effector pathway. We will focus on the recently discovered selective autophagy pathway for ER, ER-phagy, with particular emphasis on the structure and function of known mammalian ER-phagy receptors, namely FAM134B, SEC62, RTN3 and CCPG1. Finally, we conclude with our view of where the future of this field can lead our understanding of the involvement of ER-phagy in ER homeostasis.

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“…Although relatively less information is known about its biological functions compared with AND, deAND exerts no toxicity [20] and has higher oral bioavailability than that of AND [15,21]. In previous studies, the anti-cancer, anti-virus, anti-inflammation, and cardiovascular protective effects of deAND have been reported [20,[22][23][24][25][26].…”

Section: Introductionmentioning

confidence: 99%

A Diterpenoid, 14-Deoxy-11, 12-Didehydroandrographolide, in Andrographis paniculata Reduces Steatohepatitis and Liver Injury in Mice Fed a High-Fat and High-Cholesterol Diet

et al. 2020

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14-Deoxy-11,12-didehydroandrographolide (deAND), a diterpenoid in Andrographis paniculata (Burm. f.) Nees, acts as a bioactive phytonutrient that can treat many diseases. To investigate the protective effects of deAND on reducing fatty liver disease, male mice were fed a high-fat and high-cholesterol (HFHC) diet without or with 0.05% and 0.1% deAND supplementation. Cholesterol accumulation, antioxidant, and anti-inflammatory activities in liver and liver injury were evaluated after deAND treatment. The results show that deAND treatment for seven weeks reduced plasma alanine aminotransferase activity and lowered hepatic cholesterol accumulation, tumor nuclear factor-α, and histological lesions. The 0.1% deAND treatment reduced HFHC diet-induced apoptosis by lowering the caspase 3/pro-caspase 3 ratio. After 11 weeks of deAND treatment, increased NOD-like receptor protein 3 (NLRP3), capase-1, and interleukin-1β protein levels in liver were suppressed by deAND treatment. In addition, nuclear factor erythroid 2-related factor 2 (Nrf2) mRNA expression, heme oxygenase-1 protein expression, and the activities of glutathione peroxidase and glutathione reductase were increased in mice fed the HFHC diet. However, those activities of antioxidant enzymes or proteins were also upregulated by 0.1% deAND treatment. Furthermore, deAND treatment tended to lower hepatic lipid peroxides. Finally, deAND treatment reversed the depletion of hepatic glutamate level induced by the HFHC diet. These results indicate that deAND may ameliorate HFHC diet-induced steatohepatitis and liver injury by increasing antioxidant and anti-inflammatory activities.

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14-Deoxy-11,12-didehydroandrographolide induces DDIT3-dependent endoplasmic reticulum stress-mediated autophagy in T-47D breast carcinoma cells

Cited by 19 publications

References 63 publications

Cytotoxic data of 14-deoxy-11, 12-didehydroandrographolide (14-DDA), double transfection and DDIT3 silencing data in T-47D breast carcinoma cells

Cytotoxic data of 14-deoxy-11, 12-didehydroandrographolide (14-DDA), double transfection and DDIT3 silencing data in T-47D breast carcinoma cells

ER homeostasis and autophagy

A Diterpenoid, 14-Deoxy-11, 12-Didehydroandrographolide, in Andrographis paniculata Reduces Steatohepatitis and Liver Injury in Mice Fed a High-Fat and High-Cholesterol Diet

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