Opening of the CLC‐3 chloride channel induced by dihydroartemisinin contributed to early apoptotic events in human poorly differentiated nasopharyngeal carcinoma cells

2018 ◽  
Vol 119 (11) ◽  
pp. 9560-9572 ◽  
Author(s):  
Congran Zhou ◽  
Xinwei Tang ◽  
Jingkui Xu ◽  
Jiajia Wang ◽  
Yaping Yang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Chloride Channel ◽  
Carcinoma Cells ◽  
Poorly Differentiated

ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells

2012 ◽  
Vol 303 (1) ◽  
pp. C14-C23 ◽  
Author(s):  
Liwei Wang ◽  
Wenbo Ma ◽  
Linyan Zhu ◽  
Dong Ye ◽  
Yuan Li ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Chloride Channel ◽  
Cell Function ◽  
Extracellular Ph ◽  
Carcinoma Cells ◽  
Chloride Current ◽  
Disulfonic Acid ◽  
Channel Blockers ◽  
Chloride Currents ◽  
Channel Proteins

Acid-activated chloride currents have been reported in several cell types and may play important roles in regulation of cell function. However, the molecular identities of the channels that mediate the currents are not defined. In this study, activation of the acid-induced chloride current and the possible candidates of the acid-activated chloride channel were investigated in human nasopharyngeal carcinoma cells (CNE-2Z). A chloride current was activated when extracellular pH was reduced to 6.6 from 7.4. However, a further decrease of extracellular pH to 5.8 inhibited the current. The current was weakly outward-rectified and was suppressed by hypertonicity-induced cell shrinkage and by the chloride channel blockers 5-nitro-2–3-phenylpropylamino benzoic acid (NPPB), tamoxifen, and 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid disodium salt hydrate (DIDS). The permeability sequence of the channel to anions was I− > Br− > Cl− > gluconate−. Among the ClC chloride channels, ClC-3 and ClC-7 were strongly expressed in CNE-2Z cells. Knockdown of ClC-3 expression with ClC-3 small interfering (si)RNA prevented the activation of the acid-induced current, but silence of ClC-7 expression with ClC-7 siRNA did not significantly affect the current. The results suggest that the chloride channel mediating the acid-induced chloride current was volume sensitive. ClC-3 is a candidate of the channel proteins that mediate or regulate the acid-activated chloride current in nasopharyngeal carcinoma cells.

scholarly journals Proteomics-based Identification of Proteins with Altered Expression Induced by 12-O-Tetradecanoylphorbol 13-acetate in Nasopharyngeal Carcinoma CNE2 Cells

2005 ◽  
Vol 37 (2) ◽  
pp. 97-106 ◽  
Author(s):  
Pei-Zhou Jiang ◽  
Ming Gan ◽  
Hua Huang ◽  
Xin-Ming Shen ◽  
Shuang Wang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Matrix Protein ◽  
Triosephosphate Isomerase ◽  
Southern China ◽  
Carcinoma Cells ◽  
Altered Expression ◽  
Proteomics Technology ◽  
High Incidence ◽  
Apoptosis Detection ◽  
Poorly Differentiated

Abstract Nasopharyngeal carcinoma (NPC) is a malignancy with high incidence in Southern China and South-East Asia. Etiology studies indicate that chemical carcinogen promoters, such as 12-Otetradecanoylphorbol-13-acetate (TPA), are important factors causing NPC development. However, the mechanism of the TPA effect on NPC remains unclear. In the present study, cells from a poorly differentiated squamous cell carcinoma NPC cell line, CNE2, were stimulated by TPA and proteomics technology was carried out to find protein discrepancies between control and TPA-treated cells. Results revealed that TPA treatment in CNE2 cells could upregulate the expression of “triosephosphate isomerase” and “14-3-3 protein sigma” and downregulate the expression of “reticulocalbin 1 precursor”, “nucleophosmin”, “mitochondrial matrix protein p1 precursor”, and “stathmin”. The changes in the expression of these genes suggested that TPA induced CNE2 cells to antiproliferation and to apoptosis, which was confirmed by subsequent apoptosis detection. Therefore, the effects of TPA on nasopharyngeal carcinoma cells were distinct from the effects on primary epithelial cells and we suggest reasons for these differences.

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