Punicalagin induces apoptotic and autophagic cell death in human U87MG glioma cells

Wang, Shyang Guang; Huang, Ming; Li, Jui Hsiang; Lai, Fu I.; Lee, Horng Mo; Hsu, Yuan Nian

doi:10.1038/aps.2013.98

Cited by 64 publications

(59 citation statements)

References 35 publications

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“…The bioprotective effects of pomegranate juice are commonly attributed to its high concentration of polyphenols. Punicalagin (2,3-hexahydroxy-diphenoyl-4, 6-gallagyl-glucose) accounts for more than one-half of the polyphenols in pomegranate juice (Gil et al 2000), and punicalagin by itself has anti-inflammatory (JeanGilles et al 2013), anti-oxidative (Aqil et al 2012), and anti-tumor activities (Wang et al 2013). We tested punicalagin and found that this polyphenol was able to protect cultured human syncytiotrophoblasts from stress-induced apoptosis .…”

Section: Introductionmentioning

confidence: 96%

Punicalagin promotes autophagy to protect primary human syncytiotrophoblasts from apoptosis

Wang¹,

Chen²,

Longtine³

et al. 2016

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Punicalagin is a prominent polyphenol in pomegranate juice that protects cultured syncytiotrophoblasts from stress-induced apoptosis. Here, we test the hypothesis that punicalagin has this effect by inhibiting the mTOR kinase pathway to enhance autophagic turnover and limit apoptosis in cultured primary human syncytiotrophoblasts. In syncytiotrophoblasts, starvation, rapamycin, or punicalagin all decreased the expression of phosphorylated ribosomal protein S6, a downstream target of the mTOR kinase, and of the autophagy markers, LC3-II and p62. In contrast, in the presence of bafilomycin, an inhibitor of late stages of autophagy and degradation in the autophagolysosome, syncytiotrophoblasts exposed to starvation, rapamycin, or punicalagin all showed increased levels of LC3-II and p62. The number of LC3-II punctae also increased in punicalagin-treated syncytiotrophoblasts exposed to chloroquine, another inhibitor of autophagic degradation, and punicalagin increased the number of lysosomes. The apoptosis-reducing effect of punicalagin was attenuated by inhibition of autophagy using bafilomycin or knockdown of the autophagy related gene, ATG16L1. Collectively, these data support the hypothesis that punicalagin modulates the crosstalk between autophagy and apoptosis to promote survival in cultured syncytiotrophoblasts.

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Section: Introductionmentioning

confidence: 96%

Punicalagin promotes autophagy to protect primary human syncytiotrophoblasts from apoptosis

Wang¹,

Chen²,

Longtine³

et al. 2016

Reproduction

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“…6 On the other hand, PUN decreases the expression of Bcl-2 and increases the expressions of activated caspase-9 and PARP in human U87MG glioma cells. 17 Similarly, PUN induces apoptosis in human colon cancer cell lines via the intrinsic pathway with the release of cytochrome-c into the cytosol, activation of initiator caspase-9 and effector caspase-3, and down-regulation of Bcl-XL. 7 In our study, PUN significantly decreased the expression of antiapoptotic protein Bax and increased the expression of proapoptotic protein Bcl-2 in A2780 cells.…”

Section: Discussionmentioning

confidence: 99%

“…8 Furthermore, PUN increases AMPK and p27 T198 phosphorylation and then induces autophagic cell death of U87MG cells. 17 There is evidence that pomegranate juice significantly suppresses TNF->Yinduced COX-2 protein expression, NF-kB binding, and AKT activation in several cancer cell lines. In addition to these signaling pathways, the Wnt/A-catenin pathway also contributes to tumorigenesis and progression.…”

Section: Discussionmentioning

confidence: 99%

“…5,10Y15 Punicalagin has been shown to induce apoptosis in human promyelocytic leukemia HL-60 cells, HT-29 and HCT116 colon cancer lines, colon adenocarcinoma Caco-2 cells, and U87MG glioma cells. 7,16,17 Previous researches had revealed that PUN provoked the effects on various tumor cell lines: up-regulate the expression levels of Bax, 6,18 Bad, 18 cleaved-PRAP, 6,16,17 and cytochrome C 7 ; promote the activation of caspase-3 7 and caspase-9 17 ; and down-regulate the expression of Bcl-2, 6,17 Bcl-X L , 6,7,18 and cell cycle proteins such as cyclins A, 7,17 B1, 7,17 D1, 6 D2, 6 and E 6 and then regulate the proliferation and apoptosis of cancer cells.…”

Section: Among Them the Activation Of Canonical Wnt/a-catenin Signalmentioning

confidence: 99%

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Therapeutic Effects of Punicalagin Against Ovarian Carcinoma Cells in Association With β-Catenin Signaling Inhibition

Tang

Min

et al. 2016

Int J Gynecol Cancer

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“…In addition to surgery, radiotherapy or chemotherapy methods performed for the treatment of the disease, herbal treatment methods cannot be ignored. Many researchers aimed to contribute to treatment process of GBM by using herbal products (Kim et al 2008;Deng et al 2009;Hahm et al 2010;Jung & Ghil 2010;Jeong et al 2011;Wang et al 2013). However, to the best of our knowledge, studies have not yet been conducted to evaluate the activities of lichens from herbal products on GBM treatment.…”

Section: Discussionmentioning

confidence: 99%

In vitro antitumor activities of the lichen compounds olivetoric, physodic and psoromic acid in rat neuron and glioblastoma cells

Emsen

Aslan

Toğar

et al. 2015

Pharmaceutical Biology

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Context Since methods utilised in the treatment of glioblastoma multiforme (GBM) are inadequate and have too many side effects, usage of herbal products in the treatment process comes into prominence. Lichens are symbiotic organisms used for medicinal purposes for many years. There are various anticancer treatments about components of two lichen species used in the present study. Objective Antitumor potential of three lichen secondary metabolites including olivetoric acid (OLA) and physodic acid (PHA) isolated from Pseudevernia furfuracea (L.) Zopf (Parmeliaceae) and psoromic acid (PSA) isolated from Rhizoplaca melanophthalma (DC.) Leuckert (Lecanoraceae) were investigated on human U87MG-GBM cell lines and primary rat cerebral cortex (PRCC) cells for the first time. Materials and methods PRCC cells used as healthy brain cells were obtained from SpragueDawley rats. The treatments were carried out on the cells cultured for 48 h. Cytotoxic effects of different concentrations (2.5, 5, 10, 20 and 40 mg/L) of metabolites on the cells were determined via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) analyses. Total antioxidant capacity (TAC) and total oxidant status (TOS) parameters were used for assessing oxidative alterations. Oxidative DNA damage potentials of metabolites were investigated via evaluating 8-hydroxy-2 0 -deoxyguanosine (8-OH-dG) levels. Results Median inhibitory concentration (IC 50 ) values of OLA, PHA and PSA were 125.71, 698.19 and 79.40 mg/L for PRCC cells and 17.55, 410.72 and 56.22 mg/L for U87MG cells, respectively. It was revealed that cytotoxic effects of these metabolites showed positive correlation with concentration, LDH activity and oxidative DNA damage. Discussion and conclusion The present findings obtained in this study revealed that primarily OLA and then PSA had high potential for use in the treatment of GBM. ARTICLE HISTORY

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Punicalagin induces apoptotic and autophagic cell death in human U87MG glioma cells

Abstract: Punicalagin induces human U87MG glioma cell death through both apoptotic and autophagic pathways.

Cited by 64 publications

References 35 publications

Punicalagin promotes autophagy to protect primary human syncytiotrophoblasts from apoptosis

Punicalagin promotes autophagy to protect primary human syncytiotrophoblasts from apoptosis

Therapeutic Effects of Punicalagin Against Ovarian Carcinoma Cells in Association With β-Catenin Signaling Inhibition

In vitro antitumor activities of the lichen compounds olivetoric, physodic and psoromic acid in rat neuron and glioblastoma cells

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