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Ethanol Promotes Cell Migration via Activation of Chloride Channels in Nasopharyngeal Carcinoma Cells.
Alcohol Clin Exp Res 2015; 39(8):1341-51AC

Abstract

BACKGROUND

Excessive alcohol consumption has been identified as a significant risk factor for cancer development. Chloride channels have been proved previously by us and others to be involved in cancer cell migration. However, it is unknown whether chloride channels are associated with the effects of ethanol (EtOH) on cancer cell activities.

METHODS

The effects of EtOH on migration were detected by the wound healing assay in the nasopharyngeal carcinoma cells (CNE-2Z) and the normal nasopharyngeal epithelial cells (NP69-SV40T). The whole-cell patch clamp technique was used to record the EtOH-induced chloride current. The characteristics of the current were studied by anion substitution, hypertonic challenges, and channel blockers.

RESULTS

EtOH promoted the migration of cancerous CNE-2Z cells, but could hardly affect the migration of normal NP69-SV40T cells. The EtOH-induced migration could be inhibited by the chloride channel blockers, 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) and tamoxifen. The exposure of CNE-2Z cells to EtOH activated a chloride current, with the ion selectivity of I(-) >Br(-) > Cl(-) >gluconate, demonstrated by ion substitution experiments. EtOH could still activate a similar chloride current in the absence of Ca(2+) in the medium. The current could be inhibited by the hypertonicity-induced cell shrinkage and the channel blockers NPPB and tamoxifen. EtOH could also activate a chloride current in normal NP69-SV40T cells, with the properties similar to those in CNE-2Z cells, but the current density was much smaller than that recorded in cancerous CNE-2Z cells.

CONCLUSIONS

It has been demonstrated in this study that EtOH can activate chloride channels and promote cell migration in cancerous cells, but can hardly affect the activities in normal cells. The data suggest for the first time that EtOH may promote cell migration via activation of chloride channels; long-term exposure to EtOH may increase the incident of tumor metastasis.

Authors+Show Affiliations

Department of Physiology , Medical College, Jinan University, Guangzhou, China. Department of Pathophysiology, Medical College, Jinan University, Guangzhou, China.Rongcheng Hospital, Rongcheng, Shandong, China.Department of Physiology , Medical College, Jinan University, Guangzhou, China. Department of Pathophysiology, Medical College, Jinan University, Guangzhou, China.Department of Physiology , Medical College, Jinan University, Guangzhou, China. Department of Pathophysiology, Medical College, Jinan University, Guangzhou, China.Department of Physiology , Medical College, Jinan University, Guangzhou, China. Department of Pathophysiology, Medical College, Jinan University, Guangzhou, China.Department of Pathophysiology, Medical College, Jinan University, Guangzhou, China. Department of Pharmacology, Medical College, Jinan University, Guangzhou, China.Department of Physiology , Medical College, Jinan University, Guangzhou, China.Department of Physiology , Guangdong Medical College, Zhanjiang, China.Department of Pharmacology, Medical College, Jinan University, Guangzhou, China.Cardiff School of Biosciences, Cardiff University, Cardiff, United Kingdom.Department of Physiology , Medical College, Jinan University, Guangzhou, China.Department of Pharmacology, Medical College, Jinan University, Guangzhou, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26148226

Citation

Wei, Yan, et al. "Ethanol Promotes Cell Migration Via Activation of Chloride Channels in Nasopharyngeal Carcinoma Cells." Alcoholism, Clinical and Experimental Research, vol. 39, no. 8, 2015, pp. 1341-51.
Wei Y, Lin N, Zuo W, et al. Ethanol Promotes Cell Migration via Activation of Chloride Channels in Nasopharyngeal Carcinoma Cells. Alcohol Clin Exp Res. 2015;39(8):1341-51.
Wei, Y., Lin, N., Zuo, W., Luo, H., Li, Y., Liu, S., ... Chen, L. (2015). Ethanol Promotes Cell Migration via Activation of Chloride Channels in Nasopharyngeal Carcinoma Cells. Alcoholism, Clinical and Experimental Research, 39(8), pp. 1341-51. doi:10.1111/acer.12782.
Wei Y, et al. Ethanol Promotes Cell Migration Via Activation of Chloride Channels in Nasopharyngeal Carcinoma Cells. Alcohol Clin Exp Res. 2015;39(8):1341-51. PubMed PMID: 26148226.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ethanol Promotes Cell Migration via Activation of Chloride Channels in Nasopharyngeal Carcinoma Cells. AU - Wei,Yan, AU - Lin,Na, AU - Zuo,Wanhong, AU - Luo,Hai, AU - Li,Yuan, AU - Liu,Shanwen, AU - Meng,Long, AU - Fan,Aihui, AU - Zhu,Linyan, AU - Jacob,Tim J C, AU - Wang,Liwei, AU - Chen,Lixin, Y1 - 2015/07/04/ PY - 2015/03/23/received PY - 2015/05/14/accepted PY - 2015/7/7/entrez PY - 2015/7/7/pubmed PY - 2016/5/3/medline KW - Cell Migration KW - Chloride Channels KW - Ethanol KW - Patch Clamp Techniques SP - 1341 EP - 51 JF - Alcoholism, clinical and experimental research JO - Alcohol. Clin. Exp. Res. VL - 39 IS - 8 N2 - BACKGROUND: Excessive alcohol consumption has been identified as a significant risk factor for cancer development. Chloride channels have been proved previously by us and others to be involved in cancer cell migration. However, it is unknown whether chloride channels are associated with the effects of ethanol (EtOH) on cancer cell activities. METHODS: The effects of EtOH on migration were detected by the wound healing assay in the nasopharyngeal carcinoma cells (CNE-2Z) and the normal nasopharyngeal epithelial cells (NP69-SV40T). The whole-cell patch clamp technique was used to record the EtOH-induced chloride current. The characteristics of the current were studied by anion substitution, hypertonic challenges, and channel blockers. RESULTS: EtOH promoted the migration of cancerous CNE-2Z cells, but could hardly affect the migration of normal NP69-SV40T cells. The EtOH-induced migration could be inhibited by the chloride channel blockers, 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) and tamoxifen. The exposure of CNE-2Z cells to EtOH activated a chloride current, with the ion selectivity of I(-) >Br(-) > Cl(-) >gluconate, demonstrated by ion substitution experiments. EtOH could still activate a similar chloride current in the absence of Ca(2+) in the medium. The current could be inhibited by the hypertonicity-induced cell shrinkage and the channel blockers NPPB and tamoxifen. EtOH could also activate a chloride current in normal NP69-SV40T cells, with the properties similar to those in CNE-2Z cells, but the current density was much smaller than that recorded in cancerous CNE-2Z cells. CONCLUSIONS: It has been demonstrated in this study that EtOH can activate chloride channels and promote cell migration in cancerous cells, but can hardly affect the activities in normal cells. The data suggest for the first time that EtOH may promote cell migration via activation of chloride channels; long-term exposure to EtOH may increase the incident of tumor metastasis. SN - 1530-0277 UR - https://www.unboundmedicine.com/medline/citation/26148226/Ethanol_Promotes_Cell_Migration_via_Activation_of_Chloride_Channels_in_Nasopharyngeal_Carcinoma_Cells_ L2 - https://doi.org/10.1111/acer.12782 DB - PRIME DP - Unbound Medicine ER -