Sinularin induces oxidative stress‐mediated G2/M arrest and apoptosis in oral cancer cells

Wu, Chang‐Yi; Tang, Jen‐Yang; Huang, Chiung‐Yao; Liaw, Chih‐Chuang; Wu, Shih‐Hsiung; Sheu, Jyh‐Horng; Chang, Hong-Po

doi:10.1002/tox.22425

Cited by 29 publications

(35 citation statements)

References 42 publications

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“…Several natural products showed preferential killing against cancer cells and remained healthy for normal cells . For example, golden berry‐derived 4β‐hydroxywithanolide E, methanolic extracts of Solieria robusta , grape seed extracts, Cryptocarya concinna ‐derived cryptocaryone, Cinnamomum tenuifolium stem‐derived tenuifolide B, and soft coral‐derived sinularin selectively kill more oral cancer cells than normal oral cells. Therefore, drug discovery from TCM is an attractive direction for anticancer therapy.…”

Section: Introductionmentioning

confidence: 99%

Ethyl acetate extract of Nepenthes adrianii x clipeata induces antiproliferation, apoptosis, and DNA damage against oral cancer cells through oxidative stress

Tang

Peng

Cheng

et al. 2019

Environmental Toxicology

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Nepenthes plants are regarded as a kind of Traditional Chinese Medicine for several diseases but its anticancer activity remain unclear. The subject of this study is to evaluate the antiproliferation effects on oral cancer cells by Nepenthes plants using ethyl acetate extract of Nepenthes adrianii x clipeata (EANA). Cell viability was detected using MTS assay. Its detailed mechanisms including cell cycle, apoptosis, oxidative stress, and DNA damage were explored by flow cytometry or western blotting. For 24 hours EANA treatment, five kinds of oral cancer cells (CAL 27, Ca9-22, OECM-1, HSC-3, and SCC9) show IC 50 values of cell viability ranging from 8 to 17 μg/mL but the viability of normal oral cells (HGF-1) remains over 80%. Subsequently, CAL 27 and Ca9-22 cells with high sensitivity to EANA were chosen to investigate the detailed mechanism. EANA displays the time course and concentration effects for inducing apoptosis based on flow cytometry (subG1 and annexin V analyses) and western blotting [cleaved poly (ADP-ribose) polymerase (c-PARP)]. Oxidative stress and DNA damage were induced by EANA treatments in oral cancer cells through reactive oxygen species (ROS),

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Section: Introductionmentioning

confidence: 99%

Ethyl acetate extract of Nepenthes adrianii x clipeata induces antiproliferation, apoptosis, and DNA damage against oral cancer cells through oxidative stress

Tang

Peng

Cheng

et al. 2019

Environmental Toxicology

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“…Its anticancer effect has been demonstrated in human melanoma (A2058) cells [ 19 ] and gastric cancer (AGS) cells [ 20 ]. However, its selective killing effect on cancer was first shown in our previous study on oral cancer cells [ 21 ]. Here, we hypothesize that sinularin has selective killing potential against other types of cancer cells, such as breast cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Sinularin Selectively Kills Breast Cancer Cells Showing G2/M Arrest, Apoptosis, and Oxidative DNA Damage

et al. 2018

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The natural compound sinularin, isolated from marine soft corals, is antiproliferative against several cancers, but its possible selective killing effect has rarely been investigated. This study investigates the selective killing potential and mechanisms of sinularin-treated breast cancer cells. In 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H- tetrazolium, inner salt (MTS) assay, sinularin dose-responsively decreased the cell viability of two breast cancer (SKBR3 and MDA-MB-231) cells, but showed less effect on breast normal (M10) cells after a 24 h treatment. According to 7-aminoactinomycin D (7AAD) flow cytometry, sinularin dose-responsively induced the G2/M cycle arrest of SKBR3 cells. Sinularin dose-responsively induced apoptosis on SKBR3 cells in terms of a flow cytometry-based annexin V/7AAD assay and pancaspase activity, as well as Western blotting for cleaved forms of poly(ADP-ribose) polymerase (PARP), caspases 3, 8, and 9. These caspases and PARP activations were suppressed by N-acetylcysteine (NAC) pretreatment. Moreover, sinularin dose-responsively induced oxidative stress and DNA damage according to flow cytometry analyses of reactive oxygen species (ROS), mitochondrial membrane potential (MitoMP), mitochondrial superoxide, and 8-oxo-2′-deoxyguanosine (8-oxodG)). In conclusion, sinularin induces selective killing, G2/M arrest, apoptosis, and oxidative DNA damage of breast cancer cells.

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“…β-lapachone produces reactive oxygen species-mediated apoptosis in human OSCC cells [ 6 ]. In addition, recent studies demonstrated that soft coral compounds mediate ROS induced apoptosis and DNA damage in OSCC cells in vitro [ 7 , 13 ]. In the present study, we found that sandensolide-induced ROS generation and apoptosis were abolished by the antioxidant NAC, indicating that ROS is a critical mediator involved in sandensolide-induced apoptosis in OSCC.…”

Section: Discussionmentioning

confidence: 99%

“…The accumulation of DNA damage resulting from incomplete repair or disrepair may lead to DNA lesion, mutagenesis and consequently cancerous transform generation [ 5 ]. Several natural compounds targeting ROS has been reported to regulate apoptosis for selective killing in oral cancer [ 6 , 7 , 8 , 9 ]. Thus, the reduction of ROS might play a critical role in regulating the selective activation of apoptosis for selective killing in oral cancer chemotherapy.…”

Section: Introductionmentioning

confidence: 99%

Sandensolide Induces Oxidative Stress-Mediated Apoptosis in Oral Cancer Cells and in Zebrafish Xenograft Model

Chen

Liu

et al. 2018

Marine Drugs

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Presently, natural sources and herbs are being sought for the treatment of human oral squamous cell carcinoma (OSCC) in order to alleviate the side effects of chemotherapy. This study investigates the effect of sandensolide, a cembrane isolated from Sinularia flexibilis, to inhibit human OSCC cell growth with the aim of developing a new drug for the treatment of oral cancer. In vitro cultured human OSCC models (Ca9.22, SCC9 and HSC-3 cell lines) and oral normal cells (HGF-1), as well as a zebrafish xenograft model, were used to test the cytotoxicity of sandensolide (MTT assay), as well as to perform cell cycle analysis and Western blotting. Both the in vitro bioassay and the zebrafish xenograft model demonstrated the anti-oral cancer effect of sandensolide. Moreover, sandensolide was able to significantly suppress colony formation and induce apoptosis, as well as cell cycle arrest, in OSCC by regulating multiple key proteins. Induction of reactive oxygen species (ROS) was observed in sandensolide-treated oral cancer cells. However, these apoptotic changes were rescued by NAC pretreatment. These findings contribute to the knowledge of the model of action of sandensolide, which may induce oxidative stress-mediated cell death pathways as a potential agent in oral cancer therapeutics.

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Sinularin induces oxidative stress‐mediated G2/M arrest and apoptosis in oral cancer cells

Cited by 29 publications

References 42 publications

Ethyl acetate extract of Nepenthes adrianii x clipeata induces antiproliferation, apoptosis, and DNA damage against oral cancer cells through oxidative stress

Ethyl acetate extract of Nepenthes adrianii x clipeata induces antiproliferation, apoptosis, and DNA damage against oral cancer cells through oxidative stress

Sinularin Selectively Kills Breast Cancer Cells Showing G2/M Arrest, Apoptosis, and Oxidative DNA Damage

Sandensolide Induces Oxidative Stress-Mediated Apoptosis in Oral Cancer Cells and in Zebrafish Xenograft Model

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