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Emodin suppresses the nasopharyngeal carcinoma cells by targeting the chloride channels.
Biomed Pharmacother 2017; 90:615-625BP

Abstract

Emodin is a natural anthraquinone derivative isolated from the Rheum palmatum. Recent studies demonstrated that emodin has anti-cancer activity in different kinds of human cancer cell lines. However, the underlying mechanism has not been very well studied. Our previous studies showed chloride channels is an important target of anti-cancer drugs. Therefore, the purpose of this research was aimed to explore the role of chloride channels involving in the anti-cancer activity of emodin. The proliferation, cell cycle arrest and apoptosis of poorly differentiated human nasopharyngeal carcinoma cells (CNE-2Z) and normal nasopharyngeal epithelial cells (NP69-SV40T) were detected by 3-(4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide(MTT)and flow cytometry. The results indicated that emodin inhibited the CNE-2Z cell growth more significantly than NP69-SV40T cells and induced cell cycle arrest and apoptosis in CNE-2Z cells but not in NP69-SV40T cells. Chloride channel blocker 5-nitro-2-(3-phenylprop ylamino)-benzoate (NPPB) or tamoxifen both can prevent the apoptosis of CNE-2Z cells induced by emodin. Optical microscope and atomic force microscope (AFM) demonstrated that emodin can induce apoptotic volume decrease (AVD) and ultrastructure changes in CNE-2Z cell and inhibited by chloride channel blocker. These data could be a further evidence of chloride channel for preventing CNE-2Z cells from apoptosis induced by emodin. Whole cell patch clamp study also demonstrated that emodin can activate chloride channel in CNE-2Z cells but not in NP69-SV40T cells. Furthermore, the activated chloride currents can also be inhibited by chloride channel blockers indicating that chloride channel may be the potential target molecular of emodin exerting its anti-tumor efficiency in CNE-2Z cells.

Authors+Show Affiliations

Department of Pharmacology, School of Medicine, Jinan University, Guangzhou 510632, China; Research Center for Drug Discovery, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.Analysis and Test Center, Jinan University, Guangzhou 510632, China.KingMed College of Laboratory Medicine, Guangzhou, Guangdong 510200, China.Department of Pharmacology, School of Medicine, Jinan University, Guangzhou 510632, China.Department of Physiology, School of Medicine, Jinan University, Guangzhou 510632, China.Department of Pharmacology, School of Medicine, Jinan University, Guangzhou 510632, China.Department of Pharmacology, School of Medicine, Jinan University, Guangzhou 510632, China. Electronic address: linyanzhu_jnu@163.com.Department of Pathology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou 510120, China. Electronic address: yang_hf@126.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28411554

Citation

Ma, Lianshun, et al. "Emodin Suppresses the Nasopharyngeal Carcinoma Cells By Targeting the Chloride Channels." Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, vol. 90, 2017, pp. 615-625.
Ma L, Yang Y, Yin Z, et al. Emodin suppresses the nasopharyngeal carcinoma cells by targeting the chloride channels. Biomed Pharmacother. 2017;90:615-625.
Ma, L., Yang, Y., Yin, Z., Liu, M., Wang, L., Chen, L., ... Yang, H. (2017). Emodin suppresses the nasopharyngeal carcinoma cells by targeting the chloride channels. Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, 90, pp. 615-625. doi:10.1016/j.biopha.2017.03.088.
Ma L, et al. Emodin Suppresses the Nasopharyngeal Carcinoma Cells By Targeting the Chloride Channels. Biomed Pharmacother. 2017;90:615-625. PubMed PMID: 28411554.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Emodin suppresses the nasopharyngeal carcinoma cells by targeting the chloride channels. AU - Ma,Lianshun, AU - Yang,Yaping, AU - Yin,Zizhang, AU - Liu,Mei, AU - Wang,Liwei, AU - Chen,Lixin, AU - Zhu,Linyan, AU - Yang,Haifeng, Y1 - 2017/04/12/ PY - 2017/02/10/received PY - 2017/03/24/revised PY - 2017/03/26/accepted PY - 2017/4/16/pubmed PY - 2018/2/24/medline PY - 2017/4/16/entrez KW - Cell apoptosis KW - Chloride channels KW - Emodin KW - Nasopharyngeal carcinoma SP - 615 EP - 625 JF - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie JO - Biomed. Pharmacother. VL - 90 N2 - Emodin is a natural anthraquinone derivative isolated from the Rheum palmatum. Recent studies demonstrated that emodin has anti-cancer activity in different kinds of human cancer cell lines. However, the underlying mechanism has not been very well studied. Our previous studies showed chloride channels is an important target of anti-cancer drugs. Therefore, the purpose of this research was aimed to explore the role of chloride channels involving in the anti-cancer activity of emodin. The proliferation, cell cycle arrest and apoptosis of poorly differentiated human nasopharyngeal carcinoma cells (CNE-2Z) and normal nasopharyngeal epithelial cells (NP69-SV40T) were detected by 3-(4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide(MTT)and flow cytometry. The results indicated that emodin inhibited the CNE-2Z cell growth more significantly than NP69-SV40T cells and induced cell cycle arrest and apoptosis in CNE-2Z cells but not in NP69-SV40T cells. Chloride channel blocker 5-nitro-2-(3-phenylprop ylamino)-benzoate (NPPB) or tamoxifen both can prevent the apoptosis of CNE-2Z cells induced by emodin. Optical microscope and atomic force microscope (AFM) demonstrated that emodin can induce apoptotic volume decrease (AVD) and ultrastructure changes in CNE-2Z cell and inhibited by chloride channel blocker. These data could be a further evidence of chloride channel for preventing CNE-2Z cells from apoptosis induced by emodin. Whole cell patch clamp study also demonstrated that emodin can activate chloride channel in CNE-2Z cells but not in NP69-SV40T cells. Furthermore, the activated chloride currents can also be inhibited by chloride channel blockers indicating that chloride channel may be the potential target molecular of emodin exerting its anti-tumor efficiency in CNE-2Z cells. SN - 1950-6007 UR - https://www.unboundmedicine.com/medline/citation/28411554/Emodin_suppresses_the_nasopharyngeal_carcinoma_cells_by_targeting_the_chloride_channels_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0753-3322(17)30606-6 DB - PRIME DP - Unbound Medicine ER -