Corilagin induces apoptosis, autophagy and ROS generation in gastric cancer cells  in vitro

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Abstract

Corilagin, a unique component of the tannin family, has been identified in several medicinal plants. In previous literature, corilagin exhibited a marked anticancer property in a variety of human cancer cells. However, the biological effects of corilagin on gastric cancer and the mechanisms involved remain to be fully elucidated. In the present study, it was reported that corilagin induced inhibition of cell growth in SGC7901 and BGC823 cells in a concentration-dependent manner. It was found that corilagin exhibited less toxicity towards normal GES-1 cells. Furthermore, the study showed that corilagin induced the apoptosis of gastric cancer cells mainly via activating caspase-8, -9, -3 and poly ADP-ribose polymerase proteins. Simultaneously, it was verified that corilagin triggered autophagy in gastric cancer cells and the inhibition of autophagy improved the activity of corilagin on cell growth suppression. In addition, corilagin significantly increased intracellular reactive oxygen species production, which is important in inhibiting the growth of gastric cancer cells. Finally, it was shown that necroptosis cannot be induced by corilagin-incubation in SGC7901 and BGC823 cell lines. Consequently, these findings indicate that corilagin may be developed as a potential therapeutic drug for gastric cancer.

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Old, new and emerging functions of caspases.

S. Shalini, L Dorstyn, S Dawar … (2015)

Caspases are proteases with a well-defined role in apoptosis. However, increasing evidence indicates multiple functions of caspases outside apoptosis. Caspase-1 and caspase-11 have roles in inflammation and mediating inflammatory cell death by pyroptosis. Similarly, caspase-8 has dual role in cell death, mediating both receptor-mediated apoptosis and in its absence, necroptosis. Caspase-8 also functions in maintenance and homeostasis of the adult T-cell population. Caspase-3 has important roles in tissue differentiation, regeneration and neural development in ways that are distinct and do not involve any apoptotic activity. Several other caspases have demonstrated anti-tumor roles. Notable among them are caspase-2, -8 and -14. However, increased caspase-2 and -8 expression in certain types of tumor has also been linked to promoting tumorigenesis. Increased levels of caspase-3 in tumor cells causes apoptosis and secretion of paracrine factors that promotes compensatory proliferation in surrounding normal tissues, tumor cell repopulation and presents a barrier for effective therapeutic strategies. Besides this caspase-2 has emerged as a unique caspase with potential roles in maintaining genomic stability, metabolism, autophagy and aging. The present review focuses on some of these less studied and emerging functions of mammalian caspases.

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Signaling functions of reactive oxygen species.

Henry Forman, Matilde Maiorino, Fulvio Ursini (2010)

We review signaling by reactive oxygen species, which is emerging as a major physiological process. However, among the reactive oxygen species, H(2)O(2) best fulfills the requirements of being a second messenger. Its enzymatic production and degradation, along with the requirements for the oxidation of thiols by H(2)O(2), provide the specificity for time and place that are required in signaling. Both thermodynamic and kinetic considerations suggest that among possible oxidation states of cysteine, formation of sulfenic acid derivatives or disulfides can be relevant as thiol redox switches in signaling. In this work, the general constraints that are required for protein thiol oxidation by H(2)O(2) to be fast enough to be relevant for signaling are discussed in light of the mechanism of oxidation of the catalytic cysteine or selenocysteine in thiol peroxidases. While the nonenzymatic reaction between thiol and H(2)O(2) is, in most cases, too slow to be relevant in signaling, the enzymatic catalysis of thiol oxidation by these peroxidases provides a potential mechanism for redox signaling.

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Oxidative stress mediated apoptosis induced by nickel ferrite nanoparticles in cultured A549 cells.

Maqusood Ahamed, Mohd Akhtar, Maqsood Siddiqui … (2011)

Due to the interesting magnetic and electrical properties with good chemical and thermal stabilities, nickel ferrite nanoparticles are being utilized in many applications including magnetic resonance imaging, drug delivery and hyperthermia. Recent studies have shown that nickel ferrite nanoparticles produce cytotoxicity in mammalian cells. However, there is very limited information concerning the toxicity of nickel ferrite nanoparticles at the cellular and molecular level. The aim of this study was to investigate the cytotoxicity, oxidative stress and apoptosis induction by well-characterized nickel ferrite nanoparticles (size 26 nm) in human lung epithelial (A549) cells. Nickel ferrite nanoparticles induced dose-dependent cytotoxicity in A549 cells demonstrated by MTT, NRU and LDH assays. Nickel ferrite nanoparticles were also found to induce oxidative stress evidenced by generation of reactive oxygen species (ROS) and depletion of antioxidant glutathione (GSH). Further, co-treatment with the antioxidant L-ascorbic acid mitigated the ROS generation and GSH depletion due to nickel ferrite nanoparticles suggesting the potential mechanism of oxidative stress. Quantitative real-time PCR analysis demonstrated that following the exposure of A549 cells to nickel ferrite nanoparticles, the level of mRNA expressions of cell cycle checkpoint protein p53 and apoptotic proteins (bax, caspase-3 and caspase-9) were significantly up-regulated, whereas the expression of anti-apoptotic proteins (survivin and bcl-2) were down-regulated. Moreover, activities of caspase-3 and caspase-9 enzymes were also significantly higher in nickel ferrite nanoparticles exposed cells. To the best of our knowledge this is the first report showing that nickel ferrite nanoparticles induced apoptosis in A549 cells through ROS generation and oxidative stress via p53, survivin, bax/bcl-2 and caspase pathways. Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

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Author and article information

Journal

Journal ID (nlm-ta): Int J Mol Med

Journal ID (iso-abbrev): Int. J. Mol. Med

Journal ID (publisher-id): IJMM

Title: International Journal of Molecular Medicine

Publisher: D.A. Spandidos

ISSN (Print): 1107-3756

ISSN (Electronic): 1791-244X

Publication date (Print): February 2019

Publication date (Electronic): 18 December 2018

Publication date PMC-release: 18 December 2018

Volume: 43

Issue: 2

Pages: 967-979

Affiliations

[1 ]Fisheries College, Jimei University, Xiamen, Fujian 361021

[2 ]Cancer Research Center, Medical College of Xiamen University, Xiamen, Fujian 361102, P.R. China

Author notes

Correspondence to: Mr. Yuanyue Li, Fisheries College, Jimei University, 43 Yindou Road, Jimei, Xiamen, Fujian 361021, P.R. China, E-mail: 979949223@ 123456qq.com

Mr. Gang Song, Cancer Research Center, Medical College of Xiamen University, Xiang'an South Road, Xiang'an, Xiamen, Fujian 361102, P.R. China, E-mail: gangsongsd@ 123456xmu.edu.cn

Article

Publisher ID: ijmm-43-02-0967

DOI: 10.3892/ijmm.2018.4031

PMC ID: 6317684

PubMed ID: 30569134

SO-VID: 2c04c9a3-96e5-410e-b75a-6b074156da0c

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This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

Corilagin induces apoptosis, autophagy and ROS generation in gastric cancer cells in vitro

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Karger: Oncology

Most cited references 39

Old, new and emerging functions of caspases.

Signaling functions of reactive oxygen species.

Oxidative stress mediated apoptosis induced by nickel ferrite nanoparticles in cultured A549 cells.

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