Aloe-emodin, an anthraquinone, in vitro inhibits proliferation and induces apoptosis in human colon carcinoma cells

Lin, Kai-Yuan; Uen, Yih-Huei

doi:10.3892/ol_00000096

Cited by 32 publications

(40 citation statements)

References 34 publications

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“…This could be the reason for the lack of activation of caspase-3 in our experiment. There is also an issue of the elevated IC 50 values (150-220 mol/l) observed by Lin et al [11] when compared to the IC 50 of ϳ 25 mol/l observed in our study. This could be due to the differences in the percentage of FBS in the medium used for the analysis (10 vs. 2.5%).…”

Section: Discussioncontrasting

confidence: 46%

“…However, in our study we did not observe caspase-3 activation in response to treatment with AE. It is important to note that the concentration used by Lin et al [11] was 370 mol/l, compared to the much lower concentration used by us mol/l). This could be the reason for the lack of activation of caspase-3 in our experiment.…”

Section: Discussionmentioning

confidence: 99%

“…The available reports only indicate the cytotoxic activity of AE in colon cancer cells SW480, DLD-1 and HT2, but the mechanism of cell growth inhibition still remains elusive [9,10] . Lin et al [11] have reported that AE caused induction of apoptosis through the release of the apoptosis-inducing factor and cytochrome C from mitochondria, followed by the activation of caspase-3 and subsequent DNA fragmentation. However, in our study we did not observe caspase-3 activation in response to treatment with AE.…”

Section: Discussionmentioning

confidence: 99%

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Aloe Emodin Induces G2/M Cell Cycle Arrest and Apoptosis via Activation of Caspase-6 in Human Colon Cancer Cells

et al. 2012

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Aloe emodin (AE), a natural anthraquinone, is reported to have antiproliferative activity in various cancer cell lines. In this study, we analyzed the molecular mechanisms involved in the growth-inhibitory activity of this hydroxyanthraquinone in colon cancer cell, WiDr. In our observation AE inhibited cell proliferation by arresting the cell cycle at the G2/M phase and inhibiting cyclin B1. AE appreciably induced cell death specifically through the induction of apoptosis and by activating caspases 9/6. Apoptotic execution was found to be solely dependent on caspase-6 rather than caspase-3 or caspase-7. This is the first study indicating that the AE induces apoptosis specifically through the activation of caspase-6.

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Section: Discussioncontrasting

confidence: 46%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Aloe Emodin Induces G2/M Cell Cycle Arrest and Apoptosis via Activation of Caspase-6 in Human Colon Cancer Cells

et al. 2012

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“…Aloe emodin caused the release of apoptosis-inducing factor and cytochrome c from mitochondria, followed by activation of caspase-3 leading to DNA fragmentation, nuclear shrinkage and apoptosis. In addition, exposure of colon carcinoma cells to aloe emodin suppressed the casein kinase II activity in a time-dependent manner and was accompanied by a reduced phosphorylation of Bid, a downstream substrate of casein kinase II activity, the release of apoptosis-inducing factor and cytochrome c, and the caspase-3 activation are involved in aloe emodin-mediated apoptosis in colon carcinoma cells [30] . Moreover, differentiation of surviving cells toward the astrocytic lineage was confirmed by typical morphological changes and increased expression of glial fibrillary acidic protein (GFAP).…”

Section: In Vitro and Animal Studies Of Aloin And Aloe Emodinmentioning

confidence: 93%

Putative Prophylaxes of Aloe Vera for Age-Related Diseases

Yagi

2015

Journal of Gastroenterology and Hepatology Research

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The aim of the present review is focused on putative prophylaxes of Aloe vera for age-related diseases, and its check items are generally known traditional and specific diseases followed by In vitro, animal, and preliminary clinical studies: (1) prevention of cancer and alleviation of progeria; (2) prevention of cardiovascular and cerebro-vascular disorders, and inhibition of acetylcholinesterase; (3) preliminary clinical study of an aloemannose multinutrient complex on cognitive and immune functioning in Alzheimer's disease; (4) prevention of photo-aging and polycystic ovarian syndrome; (5) stimulation of periodontal fibroblasts, bone formation, and healing of pain and nephro-toxicity; and (6) anti-inflammation and immuno-response, excluding diabetic and hepatic disorders.

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“…For example, curcumin, isolated from the rhizome of Curcuma longa, demonstrates antioxidant abilities in vivo (17). Emodin, another natural anthraquinone, demonstrates protective or ameliorative effects against inflammation or oxidative stress-associated diseases (18,19). The aim of the present study is to assess the ability of emodin to alleviate the oxidative stress induced by cisplatin, and the results may elucidate the benefits of combined chemotherapy using emodin and cisplatin.…”

Section: Introductionmentioning

confidence: 99%

Emodin mitigates the oxidative stress induced by cisplatin in osteosarcoma MG63 cells

et al. 2016

Oncology Letters

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Abstract. Previously, the application of cisplatin in chemotherapy was limited due to the significant side effects on normal cell growth. In the present study, the concomitant application of emodin with cisplatin was demonstrated to ameliorate cisplatin-induced oxidative stress and markedly suppress tumor cell proliferation for the first time. Human osteosarcoma MG-63 cells were treated with cisplatin alone or in combination with emodin. The cell viability was determined by MTS assays and the augmentation of reactive oxygen species were determined by fluorogenic probes; in addition, a stable MG-63 subline bearing antioxidant response element (ARE)-driven luciferase expression was developed to monitor the activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)-ARE signaling pathway. The results indicated that cisplatin or emodin may inhibit MG-63 cell proliferation in a time-or dose-dependent manner, respectively. Concomitant treatment with cisplatin and emodin demonstrated synergic anti-tumor effects. Cisplatin augmented reactive oxygen species in the MG-63 cells, followed by the translocation of Nrf2 from the cytoplasm into the nucleus, which triggered ARE-driven luciferase expression. The addition of emodin diminished the previously described phenomenon, resulting in decreased ROS augmentation, translocation of Nrf2 and ARE-driven luciferase activity. In conclusion, emodin could ameliorate cisplatin-induced oxidative stress and protect the cells from oxidative stress-induced damage. The findings of the present study provide a novel strategy for the treatment of osteosarcoma using emodin and cisplatin.

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Aloe-emodin, an anthraquinone, in vitro inhibits proliferation and induces apoptosis in human colon carcinoma cells

Cited by 32 publications

References 34 publications

Aloe Emodin Induces G2/M Cell Cycle Arrest and Apoptosis via Activation of Caspase-6 in Human Colon Cancer Cells

Aloe Emodin Induces G2/M Cell Cycle Arrest and Apoptosis via Activation of Caspase-6 in Human Colon Cancer Cells

Putative Prophylaxes of Aloe Vera for Age-Related Diseases

Emodin mitigates the oxidative stress induced by cisplatin in osteosarcoma MG63 cells

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