Reduction of apoptosis by proanthocyanidin-induced autophagy in the human gastric cancer cell line MGC-803

Nie, Chao; Zhou, Jie; Qin, Xiaokang; Shi, Xianglin; Zeng, Qingqi; Liu, Jia; Yan, Shihai; Zhang, Lei

doi:10.3892/or.2015.4419

Cited by 28 publications

(23 citation statements)

References 64 publications

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“…However, in MGC‐803 human gastric cancer cells, PAs‐induced apoptosis was attenuated by PAs‐induced autophagy via reduction of PI3K/AKT/mTOR pathway, which was further confirmed by the addition of classical autophagy inhibitor 3‐methyladenine. After treatment with PAs (40.7 μg/mL) and 3‐methyladenine (5 mM), the inhibiton of autophagy by 3‐methyladenine could decrease Beclin 1 mRNA and increase Bcl‐2 mRNA, indicating that the block of PAs‐induced autophagy could significantly increase cell apoptosis …”

Section: Anticancer Activities and Potential Mechanismsmentioning

confidence: 99%

Recent Advances in Anticancer Activities and Drug Delivery Systems of Tannins

Cai

Zhang

Chen

et al. 2016

Medicinal Research Reviews

104

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Tannins, polyphenols in medicinal plants, have been divided into two groups of hydrolysable and condensed tannins, including gallotannins, ellagitannins, and (-)-epigallocatechin-3-gallate (EGCG). Potent anticancer activities have been observed in tannins (especially EGCG) with multiple mechanisms, such as apoptosis, cell cycle arrest, and inhibition of invasion and metastases. Furthermore, the combinational effects of tannins and anticancer drugs have been demonstrated in this review, including chemoprotective, chemosensitive, and antagonizing effects accompanying with anticancer effect. However, the applications of tannins have been hindered due to their poor liposolubility, low bioavailability, off-taste, and shorter half-life time in human body, such as EGCG, gallic acid, and ellagic acid. To tackle these obstacles, novel drug delivery systems have been employed to deliver tannins with the aim of improving their applications, such as gelatin nanoparticles, micelles, nanogold, liposomes, and so on. In this review, the chemical characteristics, anticancer properties, and drug delivery systems of tannins were discussed with an attempt to provide a systemic reference to promote the development of tannins as anticancer agents.

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Section: Anticancer Activities and Potential Mechanismsmentioning

confidence: 99%

Recent Advances in Anticancer Activities and Drug Delivery Systems of Tannins

Cai

Zhang

Chen

et al. 2016

Medicinal Research Reviews

104

View full text Add to dashboard Cite

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“…Genetic ablation of Class III PI3K leads to reflective cellular and organ damage which epitomize the essential role in regulating functional autophagy. 23 Studies on knockdown of either Class III PI3K or Beclin1 showed the decreased formation of autophagosomes through downregulated expression of LC3BII, with concomitantly increased accumulation of p62, aggregation and lipidation of LC3, and polyubiquitinated proteins showed the significant role of Class III PI3K/Beclin1 complex. 24 The proautophagic effect of Beclin1 was inhibited by the Beclin1/ Bcl-2 complex through the attenuation of the oligomerization of Beclin1/Class III PI3K complex, thereby impeding the formation of autophagosomes.…”

Section: Discussionmentioning

confidence: 99%

“…This complex subsequently stimulates the formation of autophagosomes in the foam cells. Genetic ablation of Class III PI3K leads to reflective cellular and organ damage which epitomize the essential role in regulating functional autophagy . Studies on knockdown of either Class III PI3K or Beclin1 showed the decreased formation of autophagosomes through downregulated expression of LC3BII, with concomitantly increased accumulation of p62, aggregation and lipidation of LC3, and polyubiquitinated proteins showed the significant role of Class III PI3K/Beclin1 complex .…”

Section: Discussionmentioning

confidence: 99%

Oligomeric proanthocyanidins and epigallocatechin gallate aggravate autophagy of foam cells through the activation of Class III PI3K/Beclin1‐complex mediated cholesterol efflux

et al. 2019

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Foam cells are specialized types of cells which predominate the necrotic core of atherosclerotic plaque. Recently, autophagy‐mediated cholesterol efflux from foam cells has been proposed as a beneficial therapy for atherosclerosis. The purpose of this study was to delineate the underlying molecular mechanism of oligomeric proanthocyanidins (OPC) and epigallocatechin gallate (EGCG) induced autophagy of foam cells and associated cholesterol efflux. The oxidized low‐density lipoprotein induced foam cells demonstrated impaired autophagy flux through the downregulated expressions of LC3BII/LC3BI, autophagy related gene‐5, Class III phosphoinositide 3 kinase (Class III PI3K), Beclin1, ABCA1, and ABCG1 with concomitant increase in the expressions of protein 62, Class I phosphoinositide 3 kinase, Akt, and mammalian target of rapamycin. However, these effects were significantly abolished by treatment with OPC and EGCG through activation of autophagy flux via Class III PI3K/Beclin1 and with upregulated expression of transporter proteins ABCA1 and ABCG1. Furthermore, the cholesterol efflux process in the foam cells was activated by lysosomal acid lipase and cathepsin D facilitated lipolysis of lipid droplets. Taken together, our data demonstrate that OPC and EGCG treatment stimulated the coordinated activation of autophagy and cholesterol efflux through Class III PI3K/Beclin1 pathway in foam cells, suggesting a promising therapeutic strategy against atherosclerosis.

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“…39 In addition, Chao Nie et al showed that procyanidins can induce autophagy in human gastric cancer cells but do not induce apoptosis. 40 In addition, Liao Fei showed that Euptox A has good antitumor activity. 41 Based on these data, we believe that Euptox A has the potential for use as a drug that promotes autophagy (similar to temozolomide) to kill apoptosis-resistant tumor cells by autophagic death.…”

Section: Discussionmentioning

confidence: 99%

Euptox A Induces G1 Arrest and Autophagy via p38 MAPK- and PI3K/Akt/mTOR-Mediated Pathways in Mouse Splenocytes

Weng

et al. 2017

J Histochem Cytochem.

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Euptox A (9-oxo-10, 11-dehydroageraphorone), the main toxin isolated from Eupatorium adenophorum, is known to induce immunotoxicity in animals. However, the precise mechanism underlying the effects of Euptox A on splenocytes is unclear. Here, we aimed to investigate the molecular mechanisms underlying the effect of Euptox A in mouse spleens after its intragastric administration and found that Euptox A exhibits proautophagic effects in splenocytes. Euptox A markedly arrested the splenocytes in the G0/G1 phase, which was accompanied by inhibition of the expression of the positive regulators CDK4, CDK2, cyclin D1, PCNA, and E2F1, and promotion of the expression of the negative regulators p53, p21 Waf1/Cip1, p27 Kip1, and Chk1. We also found that Euptox A did not markedly induce splenocyte apoptosis, but induced autophagy while increasing the subcellular localization of punctate LC3, ratio of LC3-II/LC3-I, and Beclin 1 levels, and decreasing p62 levels. Euptox A also significantly inhibited p-PI3K, p-p38 MAPK, p-Akt, and p-mTOR expression, but increased PTEN and p-AMPK expression. These results indicated that Euptox A induced splenocyte autophagy by inhibiting the PI3K/Akt/mTOR pathway, suppressing p38 MAPK expression, and activating AMPK. These findings provide new insights into the mechanisms involved in spleen toxicity caused by Euptox A in mice.

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Reduction of apoptosis by proanthocyanidin-induced autophagy in the human gastric cancer cell line MGC-803

Cited by 28 publications

References 64 publications

Recent Advances in Anticancer Activities and Drug Delivery Systems of Tannins

Recent Advances in Anticancer Activities and Drug Delivery Systems of Tannins

Oligomeric proanthocyanidins and epigallocatechin gallate aggravate autophagy of foam cells through the activation of Class III PI3K/Beclin1‐complex mediated cholesterol efflux

Euptox A Induces G1 Arrest and Autophagy via p38 MAPK- and PI3K/Akt/mTOR-Mediated Pathways in Mouse Splenocytes

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