Emodin elicits cytotoxicity in human lung adenocarcinoma A549 cells through inducing apoptosis

Li, Wing-Yan; Ng, Yam-Fung; Zhang, Huan; Guo, Zi-Dong; Guo, De-Jian; Kwan, Yiu Wa; Leung, George Pak-Heng; Lee, Simon Ming‐Yuen; Yu, Peter H.; Chan, Shun‐Wan

doi:10.1007/s10787-013-0186-4

Cited by 30 publications

(18 citation statements)

References 34 publications

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“…Emodin is derived from rhubarb and numerous other plants, and has demonstrated antibacterial, antiviral, anti-inflammatory and anticancer effects (15). However, previous studies have revealed that emodin inhibits cell growth in several types of cancer cells by regulating genes related to apoptosis, oncogenesis, proliferation and cancer cell invasion and metastasis (10,16,17). Notably, emodin inhibited epithelial-mesenchymal transition, suggesting that emodin may have anticancer effects (18).…”

Section: Discussionmentioning

confidence: 99%

Emodin induces apoptosis of human breast cancer cells by modulating the expression of apoptosis-related genes

Zhang

Hou

et al. 2015

Oncology Letters

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Abstract. The aim of this study was to investigate the effects of emodin on the proliferation of human breast cancer cells . Cell viability following emodin treatment was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The effects of emodin on apoptosis were determined by flow cytometry using Annexin V-fluorescein isothiocyanate and propidium iodide staining. Quantitative polymerase chain reaction and western blot analysis were used to determine changes in the expression of apoptotic genes and protein, respectively. The effect of emodin on the invasiveness of breast cancer cells was evaluated by Matrigel invasion assay. Treatment of breast cancer cells Bcap-37 and ZR-75-30 with emodin was observed to inhibit the growth and induced apoptosis in a time-and dose-dependent manner. Emodin reduced the level of Bcl-2 and increased levels of cleaved caspase-3, PARP, p53 and Bax. These findings indicate that emodin induces growth inhibition and apoptosis in human breast cancer cells. Emodin may be a potential therapeutic agent for the treatment of breast cancer. IntroductionBreast cancer is a common malignant tumor and accounts for the majority of cancer mortality in females (1). Breast cancer has an estimated incidence of 1,676,633 and had an estimated mortality rate of 521,817 in 2012 worldwide (2). In China, there has been an increasing incidence of breast cancer in recent decades (3). In 2012, it was estimated that ~48,000 females would succumb to breast cancer. To date, chemotherapy has been the mainstay for the treatment of breast cancer. However, the side effects and drug resistance associated with chemotherapy have limited its effectiveness for the treatment of breast cancer (4,5). A number of natural extractions have demonstrated a wide range of biological activity and low toxicity in animal models, and have been considered as an alternative method of breast cancer treatment (6,7).Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is a biologically active anthraquinone identified in the roots and bark of a number of plants. Emodin is also observed naturally in a number of widely used Chinese medicinal herbs, including Rheum officinale (8) and Polygonam cuspidatummedicine (9). It has been widely studied for its antibacterial, diuretic, immuno suppressive, anti-inflammatory and vaso relaxant effects. It has been reported that emodin induces apoptosis of several types of human cancer cells (10-13) by modulating various signaling pathways. However, the biological mechanisms by which emodin induces cytotoxicity remain largely unknown. Furthermore, the biological effects of emodin on breast cancer cells remain to be determined.In this study, the effects of emodin on the proliferation and apoptosis of breast cancer cells were assessed. In addition, the mechanism by which emodin mediates these biological effects was elucidated. We demonstrated that emodin inhibited the proliferation and induced apoptosis of Bcap-37 and ZR-75-30 breast cancer cells. These observations suggest that emodi...

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Section: Discussionmentioning

confidence: 99%

Emodin induces apoptosis of human breast cancer cells by modulating the expression of apoptosis-related genes

Zhang

Hou

et al. 2015

Oncology Letters

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“…In another study, emodin (IC 50 = 3.70 µ m ) was shown to modulate the expression of apoptosis‐related genes to induce growth inhibition and apoptosis in A549 cells. Treatment with emodin helped to enhance apoptosis in A549 cells through up‐regulation of the gene expression of Fas ligand (FASL) and disabled damage repair in A549 cells through down‐regulation of the gene expression of C‐MYC (Li et al ., ). Emodin could induce growth inhibition and apoptosis in MCF‐7 cells through the modulation of the expression of apoptosis‐related genes.…”

Section: Pharmacologymentioning

confidence: 97%

Emodin: A Review of its Pharmacology, Toxicity and Pharmacokinetics

Dong

Yin

et al. 2016

Phytotherapy Research

549

365

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Emodin is a natural anthraquinone derivative that occurs in many widely used Chinese medicinal herbs, such as Rheum palmatum, Polygonum cuspidatum and Polygonum multiflorum. Emodin has been used as a traditional Chinese medicine for over 2000 years and is still present in various herbal preparations. Emerging evidence indicates that emodin possesses a wide spectrum of pharmacological properties, including anticancer, hepatoprotective, antiinflammatory, antioxidant and antimicrobial activities. However, emodin could also lead to hepatotoxicity, kidney toxicity and reproductive toxicity, particularly in high doses and with long-term use. Pharmacokinetic studies have demonstrated that emodin has poor oral bioavailability in rats because of its extensive glucuronidation. This review aims to comprehensively summarize the pharmacology, toxicity and pharmacokinetics of emodin reported to date with an emphasis on its biological properties and mechanisms of action. Copyright © 2016 John Wiley & Sons, Ltd.

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“…In these experiments, treatment with essential oil of C. sylvestris at 4.0 µg/ml reduced the colony-forming ability of A549 cells to 6% of the value obtained with the control. This effect could be due to interference of essential oil in the membrane integrity, DNA fragmentation or mitochondrial depolarization (Li et al, 2014;Ruan et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

DNA damages promoted by the essential oil from leaves of Casearia sylvestris Sw. (Salicaceae)

Pereira¹,

Marquete²,

Cruz³

et al. 2016

J. Med. Plants Res.

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The Casearia species (Salicaceae) occur in the tropics and subtropics and their extracts are rich in clerodane-type diterpenes, known as casearins. According to the literature, extracts from Casearia sylvestris exhibit cytotoxic and genotoxic effects in different tumor cell lines, possibly related to the casearins. On the other hand, there are few studies related to the DNA damages of the essential oils from this species. This study is aimed at evaluating DNA damages promoted by the essential oil from leaves of C. sylvestris collected in Rio de Janeiro. The essential oil was obtained from fresh leaves (1.5 kg) by hydrodistillation for 2 h in a Clevenger-type apparatus, and analyzed both by gas chromatography coupled to a mass spectrometer (GC-MS) and gas chromatography coupled to a flame ionization detector (GC-FID). These analyses revealed a very diversified (n = 21 compounds) volatile fraction composed mainly of non-oxygenated sesquiterpenes (72.1%), and the major component was identified as α-humulene (17.8%). Genotoxicity was evaluated by the comet assay, showing DNA damages, mainly of classes 3 and 4 at 4.0 µg/ml (p < 0.05) according to the damage index (DI). This is the first demonstration of DNA damages in response to the essential oil of C. sylvestris.

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Emodin elicits cytotoxicity in human lung adenocarcinoma A549 cells through inducing apoptosis

Cited by 30 publications

References 34 publications

Emodin induces apoptosis of human breast cancer cells by modulating the expression of apoptosis-related genes

Emodin induces apoptosis of human breast cancer cells by modulating the expression of apoptosis-related genes

Emodin: A Review of its Pharmacology, Toxicity and Pharmacokinetics

DNA damages promoted by the essential oil from leaves of Casearia sylvestris Sw. (Salicaceae)

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