Anticancer effects of 4-vinyl-2,6-dimethoxyphenol (canolol) against SGC-7901 human gastric carcinoma cells

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Abstract

Gastric cancer remains the fourth most commonly diagnosed cancer and is the second leading cause of cancer-related mortality worldwide. The aim of this study was to investigate the effects of canolol on the proliferation and apoptosis of SGC-7901 human gastric cancer cells and its relevant molecular mechanisms. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to observe the effect of canolol on the proliferation of SGC-7901 human gastric adenocarcinoma cells. The results showed that SGC-7901 cells exhibited a marked dose-dependent reduction in the proliferation rate. The survival rate of the cells was 88.86±1.58% at 50 μmol/l, decreasing to 53.73±1.51% at 800 μmol/l (P<0.05). By contrast, canolol had no significant toxicity on the human gastric mucosal epithelial cell line GES-1. The vivid images of cell morphology using an inverted microscope provided confirmation of the MTT assay. Treatment of SGC-7901 cells with canolol resulted in apoptosis demonstrated by flow cytometry. Furthermore, canolol downregulated the mRNA levels of COX-2, but had no significant effect on the mRNA expession of the Bax and Bcl-2 genes. These findings suggest that canolol has potential to be developed as a new natural anti-gastric carcinoma agent.

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Most cited references 33

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The cyclooxygenase (COX)-2 gene encodes an inducible prostaglandin synthase enzyme that is overexpressed in adenocarcinomas and other tumors. Deletion of the murine Cox-2 gene in Min mice reduced the incidence of intestinal tumors, suggesting that it is required for tumorigenesis. However, it is not known if overexpression of Cox-2 is sufficient to induce tumorigenic transformation. We have derived transgenic mice that overexpress the human COX-2 gene in the mammary glands using the murine mammary tumor virus promoter. The human Cox-2 mRNA and protein are expressed in mammary glands of female transgenic mice and were strongly induced during pregnancy and lactation. Female virgin Cox-2 transgenic mice showed precocious lobuloalveolar differentiation and enhanced expression of the beta-casein gene, which was inhibited by the Cox inhibitor indomethacin. Mammary gland involution was delayed in Cox-2 transgenic mice with a decrease in apoptotic index of mammary epithelial cells. Multiparous but not virgin females exhibited a greatly exaggerated incidence of focal mammary gland hyperplasia, dysplasia, and transformation into metastatic tumors. Cox-2-induced tumor tissue expressed reduced levels of the proapoptotic proteins Bax and Bcl-x(L) and an increase in the anti-apoptotic protein Bcl-2, suggesting that decreased apoptosis of mammary epithelial cells contributes to tumorigenesis. These data indicate that enhanced Cox-2 expression is sufficient to induce mammary gland tumorigenesis. Therefore, inhibition of Cox-2 may represent a mechanism-based chemopreventive approach for carcinogenesis.

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Numsen Hail Jr., Reuben Lotan, Shi-yong R Sun (2004)

Cancer chemopreventive agents are typically natural products or their synthetic analogs that inhibit the transformation of normal cells to premalignant cells or the progression of premalignant cells to malignant cells. These agents are believed to function by modulating processes associated with xenobiotic biotransformation, with the protection of cellular elements from oxidative damage, or with the promotion of a more differentiated phenotype in target cells. However, an increasing number of chemopreventive agents (e.g., certain retinoids, nonsteroidal anti-inflammatory drugs, polyphenols, and vanilloids) have been shown to stimulate apoptosis in premalignant and malignant cells in vitro or in vivo. Apoptosis is arguably the most potent defense against cancer because it is the mechanism used by metazoans to eliminate deleterious cells. Many chemopreventive agents appear to target signaling intermediates in apoptosis-inducing pathways. Inherently, the process of carcinogenesis selects against apoptosis to initiate, promote, and perpetuate the malignant phenotype. Thus, targeting apoptosis pathways in premalignant cells--in which these pathways are still relatively intact--may be an effective method of cancer prevention. In this review, we construct a paradigm supporting apoptosis as a novel target for cancer chemoprevention by highlighting recent studies of several chemopreventive agents that engage apoptosis pathways.

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Author and article information

Journal

Journal ID (nlm-ta): Oncol Lett

Journal ID (iso-abbrev): Oncol Lett

Journal ID (publisher-id): OL

Title: Oncology Letters

Publisher: D.A. Spandidos

ISSN (Print): 1792-1074

ISSN (Electronic): 1792-1082

Publication date (Print): May 2013

Publication date (Electronic): 05 March 2013

Publication date PMC-release: 05 March 2013

Volume: 5

Issue: 5

Pages: 1562-1566

Affiliations

[1 ]Division of Clinical Epidemiology, First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China;

[2 ]Division of Pathology, School of Medicine, Fujita Health University, Toyoake, Japan;

[3 ]Department of Pathogeny Biology, Norman Bethune Medical College of Jilin University, Changchun, Jilin 130021, P.R. China

[4 ]Department of Gastric and Colorectal Surgery, First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China

Author notes

Correspondence to: Dr Xue-Yuan Cao, Department of Gastric and Colorectal Surgery, First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China, E-mail: ccmzc32jdyycao@ 123456yahoo.com.cn

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Publisher ID: ol-05-05-1562

DOI: 10.3892/ol.2013.1230

PMC ID: 3678703

PubMed ID: 23761819

SO-VID: bc218fe4-74d4-4d2f-ad81-503d706dfc20

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This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

Anticancer effects of 4-vinyl-2,6-dimethoxyphenol (canolol) against SGC-7901 human gastric carcinoma cells

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Abstract

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Karger: Oncology

Most cited references 33

Cell death in development.

Overexpression of cyclooxygenase-2 is sufficient to induce tumorigenesis in transgenic mice.

Apoptosis as a novel target for cancer chemoprevention.

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