Allicin Induces Anti-human Liver Cancer Cells through the p53 Gene Modulating Apoptosis and Autophagy

Chu, Yung Lin; Ho, Chi Tang; Chung, Jing Gung; Raghu, Rajasekaran; Lo, Yi Chen; Sheen, Lee‐Yan

doi:10.1021/jf403241s

Cited by 109 publications

(77 citation statements)

References 31 publications

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“…Cells (5×10 4 cells/ml) were plated in a 12-well plate and treated with fisetin (40 μM) for 0, 12, 24 and 48 hours and then fixed in 3% methanol in PBS at room temperature for 20 min. Cells were stained with DAPI solution (2 μg/ml) and photographed under fluorescence microscopy as described previously (31). Nuclear condensation of cells relative to total cells was evaluated, with a minimum of 150 cells/field and at least three fields in each well being counted.…”

Section: Methodsmentioning

confidence: 99%

“…In brief, HSC3 cells (5×10 4 cells/ml) were plated in a 12-well plate and treated with 40 μM of fisetin for 0, 6, 24 and 48 h then cells were harvested and re-suspended in 25 μl of 10 μM substrate solution containing PhiPhiLux-G 1 D 1 for caspase-3, or CaspaLux8-L 1 D 2 for caspase-8 or CaspaLux9-M 1 D 2 (both from OncoImmunin, Gaithersburg, MD, USA) for caspase-9 determination before being incubated at 37˚C for 60 min. After incubation, all samples were washed with PBS and caspase activities were analyzed by flow cytometry as described previously (31,32,36).…”

Section: Methodsmentioning

confidence: 99%

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Fisetin Induces Apoptosis of HSC3 Human Oral Cancer Cells Through Endoplasmic Reticulum Stress and Dysfunction of Mitochondria-mediated Signaling Pathways

Shih

Hung

Lee

et al. 2017

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Abstract. Background Western blotting was used to examine the levels of apoptotic-associated protein and results indicated that fisetin increased expression of pro-apoptotic proteins such as B-cell lymphoma 2 (BCL2) antagonist/killer (BAK) and BCL2-associated X (BAX) but reduced that of anti-apoptotic protein such as BCL2 and BCL-x, and increased the cleaved forms of caspase-3, -8 and -9, and cytochrome c, apoptosis-inducing factor (AIF) and endonuclease G (ENDO G) in HSC3 cells. Confocal microscopy showed that fisetin increased the release of cytochrome c, AIF and ENDO G from mitochondria into the cytoplasm. Conclusion: Based on these observations, we suggest that fisetin induces apoptotic cell death through endoplasmic reticulum stress-and mitochondria-dependent pathways.Oral cancer is a subtype of head and neck squamous cell carcinoma. Oral squamous cell carcinoma (OSCC) comprises of a large proportion of head and neck SCC (1). In men, oral cancer constitutes approximately 3% of all malignant 1103

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Fisetin Induces Apoptosis of HSC3 Human Oral Cancer Cells Through Endoplasmic Reticulum Stress and Dysfunction of Mitochondria-mediated Signaling Pathways

Shih

Hung

Lee

et al. 2017

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“…Allicin, an organic sulfide from garlic Allium sativum, was found to exhibit antiproliferative effects on colon cancer, glioma and hepatocellular carcinoma cells, as reviewed in [213, 214]. Allicin can induce death of human hepatocellular carcinoma HepG2 cells through the reduced TP53 expression in the cytoplasm, inhibited PI3K/mTOR signaling pathway, reduced BCL-2 expression and enhanced AMPK/TSC2 and BECN1 pathways, as indicated in [215, 216]. …”

Section: Anticancer Natural Compounds and Autophagymentioning

confidence: 99%

Natural Compounds As Modulators of Non-apoptotic Cell Death in Cancer Cells

Guamán-Ortiz

Orellana²,

Ratovitski³

2017

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Cell death is an innate capability of cells to be removed from microenvironment, if and when they are damaged by multiple stresses. Cell death is often regulated by multiple molecular pathways and mechanism, including apoptosis, autophagy, and necroptosis. The molecular network underlying these processes is often intertwined and one pathway can dynamically shift to another one acquiring certain protein components, in particular upon treatment with various drugs. The strategy to treat human cancer ultimately relies on the ability of anticancer therapeutics to induce tumor-specific cell death, while leaving normal adjacent cells undamaged. However, tumor cells often develop the resistance to the drug-induced cell death, thus representing a great challenge for the anticancer approaches. Numerous compounds originated from the natural sources and biopharmaceutical industries are applied today in clinics showing advantageous results. However, some exhibit serious toxic side effects. Thus, novel effective therapeutic approaches in treating cancers are continued to be developed. Natural compounds with anticancer activity have gained a great interest among researchers and clinicians alike since they have shown more favorable safety and efficacy then the synthetic marketed drugs. Numerous studies in vitro and in vivo have found that several natural compounds display promising anticancer potentials. This review underlines certain information regarding the role of natural compounds from plants, microorganisms and sea life forms, which are able to induce non-apoptotic cell death in tumor cells, namely autophagy and necroptosis.

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“…Allicin has been extensively studied for its wide range of biological activities, including anticancer effect [13][14][15]. It has obvious inhibitory effects on different kinds of tumor cells, such as gastric cancer [16][17][18][19], colon cancer [20], glioblastoma [21], liver cancer [22,23], ovarian cancer [24], and pancreatic cancer [25], and has been put into clinical treatment as an aid cancer drug. A newly issued report shows that allicin, combined with cyclophosphamide, can improve the efficiency on neuroblastomabearing mice [26].…”

Section: Introductionmentioning

confidence: 99%

Role of p38 MAPK activation and mitochondrial cytochrome-c release in allicin-induced apoptosis in SK-N-SH cells

Zhuang

Chi

2016

Anti-Cancer Drugs

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Here, we investigate the apoptotic effect of allicin, the predominant component of freshly crushed garlic, on neuroblastoma cells. In this paper, the authors have first assessed the effect of allicin on human neuroblastoma SK-N-SH cells and then investigated the underlying mechanism. The results indicate that allicin suppresses SK-N-SH cell growth in a dose-dependent and time-dependent manner and that 5 μmol/l of allicin leads to a significant increase in apoptotic rate with annexin-V/PI double staining. Western blot analysis shows that treatment with allicin-induced apoptosis through activation of caspases-3 and 9. Phosphorylation of p38 MAPK contributes to allicin-induced apoptosis upstream of caspase activation. Using p38 MAPK inhibitor, the authors discovered that p38 MAPK activation subsequently induces the release of cytochrome-c from mitochondria into the cytosol. Taken together, the results demonstrate that allicin can activate the p38 MAPK pathway, which leads to mitochondrial release of cytochrome-c, thus inducing SK-N-SH cell apoptosis. Overall, this study suggests that allicin may be used as one of the novel pharmacological treatment strategies in neuroblastoma.

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Allicin Induces Anti-human Liver Cancer Cells through the p53 Gene Modulating Apoptosis and Autophagy

Cited by 109 publications

References 31 publications

Fisetin Induces Apoptosis of HSC3 Human Oral Cancer Cells Through Endoplasmic Reticulum Stress and Dysfunction of Mitochondria-mediated Signaling Pathways

Fisetin Induces Apoptosis of HSC3 Human Oral Cancer Cells Through Endoplasmic Reticulum Stress and Dysfunction of Mitochondria-mediated Signaling Pathways

Natural Compounds As Modulators of Non-apoptotic Cell Death in Cancer Cells

Role of p38 MAPK activation and mitochondrial cytochrome-c release in allicin-induced apoptosis in SK-N-SH cells

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