Curcumin induces autophagic cell death in Spodoptera frugiperda cells

Veeran, Sethuraman; Shu, Benshui; Cui, Gaofeng; Fu, Shengjiao; Zhong, Guohua

doi:10.1016/j.pestbp.2017.05.004

Cited by 27 publications

(21 citation statements)

References 26 publications

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“…Given that malignant glioma has a poor prognosis (Zanotto-Filho et al ., 2015; Klinger and Mittal, 2016) and curcumin-mediated anticancer activity is associated with cell growth inhibition and the induction of apoptosis and autophagy (Klinger and Mittal, 2016; Lee et al ., 2016; Zhang et al ., 2016; Li et al ., 2017; Veeran et al ., 2017), we observed changes in curcumin-induced cell death and autophagy in A172 human glioblastoma cells. Cell viability was measured with the MTT assay (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…It also has anticancer activity, affecting tumor initiation, proliferation, progression, metastasis, invasion, and angiogenesis (Kawamori et al ., 1999; Kunnumakkara et al ., 2008). Curcumin-mediated anticancer activity is associated with the inhibition of cell growth and the induction of apoptosis and autophagy (Klinger and Mittal, 2016; Lee et al ., 2016; Zhang et al ., 2016; Li et al ., 2017; Veeran et al ., 2017). Curcumin induces autophagy and apoptosis in human gastric cancer cells (Li et al ., 2017; Fu et al ., 2018), human colon cancer cells (Zhang et al ., 2016), brain tumor cells (Zanotto-Filho et al ., 2015), and Sf9 insect cells (Veeran et al ., 2017).…”

Section: Introductionmentioning

confidence: 99%

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Curcumin-Induced Autophagy Augments Its Antitumor Effect against A172 Human Glioblastoma Cells

Lee

Yoon

Moon

2019

Biomolecules & Therapeutics

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Glioblastoma is the most aggressive common brain tumor in adults. Curcumin, from Curcuma longa , is an effective antitumor agent. Although the same proteins control both autophagy and cell death, the molecular connections between them are complicated and autophagy may promote or inhibit cell death. We investigated whether curcumin affects autophagy, which regulates curcumin-mediated tumor cell death in A172 human glioblastoma cells. When A172 cells were incubated with 10 μM curcumin, autophagy increased in a time-dependent manner. Curcumin-induced cell death was reduced by co-incubation with the autophagy inhibitors 3-methyladenine (3-MA), hydroxychloroquine (HCQ), and LY294002. Curcumin-induced cell death was also inhibited by co-incubation with rapamycin, an autophagy inducer. When cells were incubated under serum-deprived medium, LC3-II amount was increased but the basal level of cell viability was reduced, leading to the inhibition of curcumin-induced cell death. Cell death was decreased by inhibiting curcumin-induced autophagy using small interference RNA (siRNA) of Atg5 or Beclin1. Therefore, curcumin-mediated tumor cell death is promoted by curcumin-induced autophagy, but not by an increase in the basal level of autophagy in rapamycin-treated or serum-deprived conditions. This suggests that the antitumor effects of curcumin are influenced differently by curcumin-induced autophagy and the prerequisite basal level of autophagy in cancer cells.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Curcumin-Induced Autophagy Augments Its Antitumor Effect against A172 Human Glioblastoma Cells

Lee

Yoon

Moon

2019

Biomolecules & Therapeutics

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“…Thus, we do not have a strong basis from which to conclude that our observed decline in fluorescence indicates promotion of cell death. An alternative explanation may be found in the well-documented stimulatory effect of curcumin [35–39] and its post-hepatic metabolite tetrahydrocurcumin [40] on autophagy. Autophagy is a physiological process which facilitates organized disassembly of damaged proteins and organelles in order to preserve energy balance and tissue homeostasis [41].…”

Section: Discussionmentioning

confidence: 99%

A biological extract of turmeric (Curcuma longa) modulates response of cartilage explants to lipopolysaccharide

Pearson

Kott

2019

BMC Complement Altern Med

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Background Turmeric is commonly used as a dietary treatment for inflammation, but few studies have evaluated the direct effect of turmeric on cartilage. The purpose of this study was to characterize cartilage explants’ inflammatory responses to lipopolysaccharide in the presence of a simulated biological extract of turmeric. Methods Turmeric was incubated in simulated gastric and intestinal fluid, followed by inclusion of liver microsomes and NADPH. The resulting extract (TURsim) was used to condition cartilage explants in the presence or absence of lipopolysaccharide. Explants were cultured for 96 h (h); the first 24 h in basal tissue culture media and the remaining 72 h in basal tissue culture media containing TURsim (0, 3, 9 or 15 μg/mL). Lipopolysaccharide (0 or 5 μg/mL) was added for the final 48 H. media samples were collected immediately prior to lipopolysaccharide exposure (0 h) and then at 24 and 48 h after, and analyzed for prostaglandin E2 (PGE2), glycosaminoglycan (GAG), and nitric oxide (NO). Explants were stained with calcein-AM for an estimate of live cells. Data were analyzed using a 2-way repeated measures (GAG, PGE2, NO) or 1-way ANOVA without repeated measures (viability). Significance accepted at p < 0.05. Results TURsim significantly reduced PGE2, NO and GAG, and calcein fluorescence was reduced. Conclusions: These data contribute to the growing body of evidence for the utility of turmeric as an intervention for cartilage inflammation.

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“…Secondary antibody Alexa Fluor 488 (A-11008) was purchased from Thermo Fisher Scientific (Waltham, MA). Production of Sf9-Atg8 antibody and sequence details are published in our earlier paper, 6 GenBank ID: MF069154.1.…”

Section: Methodsmentioning

confidence: 99%

“…Among the ATG genes, ATG8 is mainly important because they play important key regulators of autophagic cell death and are used as autophagy markers. 11 Sf9-Atg8 sequence details were published in our earlier paper 6 and GenBank ID: MF069154.1.…”

Section: Introductionmentioning

confidence: 99%

Curcumin‐induced autophagy and nucleophagy in Spodoptera frugiperda Sf9 insect cells occur via PI3K/AKT/TOR pathways

Veeran

Cui

Shu

et al. 2018

J of Cellular Biochemistry

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Compounds from plants or microbes are important resources for new natural pesticides against a wide variety of pests. The growing attention on the role of autophagy (type II cell death) in regulation of insect toxicology has propelled researchers to investigate autophagic cell death pathways. Our previous study proved that the cytotoxic effect of curcumin in Spodoptera frugiperda cells is regulated by autophagy. However, the signaling pathways and molecular mechanisms had not been determined. The current study elucidates curcumin inhibition of survival signaling by blocking the activation of PI3K/AKT/TOR pathways to induce autophagy in S. frugiperda cells. The result demonstrates that nucleophagy associated with cell death following the curcumin treatment. Following the curcumin treatment, Atg8/LC3 immunostaining in both nucleus and cytoplasm was markedly increased. Further, messenger RNA expression level of Atg8 and Atg1 genes regulation by curcumin was examined using quantitative reverse transcription polymerase chain reaction, and the result exhibited increased level of expression after curcumin treatment in a time‐dependent manner. Our current study provides new insights to the autophagy occurring via PI3K/AKT/TOR pathways in S. frugiperda Sf9 insect cells induced by curcumin. Taken together, our results show for the first time that curcumin induced nucleophagy in lepidopteron insect cell line.

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Curcumin induces autophagic cell death in Spodoptera frugiperda cells

Cited by 27 publications

References 26 publications

Curcumin-Induced Autophagy Augments Its Antitumor Effect against A172 Human Glioblastoma Cells

Curcumin-Induced Autophagy Augments Its Antitumor Effect against A172 Human Glioblastoma Cells

A biological extract of turmeric (Curcuma longa) modulates response of cartilage explants to lipopolysaccharide

Curcumin‐induced autophagy and nucleophagy in Spodoptera frugiperda Sf9 insect cells occur via PI3K/AKT/TOR pathways

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