目的 探討阿司匹林對人鼻咽癌CNE-1、5-8F細胞增殖、遷移與侵襲的影響和機制。方法 將人鼻咽癌CNE-1、5-8F細胞株分為對照組和阿司匹林（0.00、1.25、2.50、5.00、10.00mmol/L）處理組。噻唑藍（MTT）法檢測不同濃度阿司匹林作用24、48、72h后對CNE-1、5-8F細胞的增殖能力，以半數(shù)抑制濃度（IC₅₀）作為后續(xù)實驗藥物處理濃度。集落形成實驗檢測CNE-1和5-8F細胞增殖能力，Transwell實驗檢測CNE-1和5-8F細胞遷移及侵襲能力的變化，Western blotting法檢測CNE-1和5-8F細胞中蛋白激酶B（Akt）、磷脂酰肌醇3-激酶（PI3K）、波形蛋白（Vimentin）、E-鈣黏蛋白（E-cadherin）、Snail蛋白相對表達水平。結(jié)果 人鼻咽癌CNE-1、5-8F細胞分別經(jīng)1.25、2.50、5.00、10.00mmol/L阿司匹林處理后，細胞增殖均受到不同程度抑制，且呈時間及濃度相關(guān)性，IC₅₀分別為3.3、2.7mmol/L。與對照組相比，經(jīng)阿司匹林處理后，鼻咽癌CNE-1、5-8F細胞的細胞增殖和集落形成能力明顯下降（P＜0.01）。與對照組相比，經(jīng)阿司匹林處理后，劃痕愈合率顯著降低（P＜0.05）。Trasnwell遷移實驗結(jié)果表明，與對照組相比，阿司匹林處理組鼻咽癌細胞CNE-1和5-8F 48h穿過小室的數(shù)目顯著減少（P＜0.05、0.001）。與對照組相比，阿司匹林處理組CNE-1、5-8F細胞的E-cadherin蛋白表達顯著增加（P＜0.05），PI3K、Akt、Vimentin、Snail蛋白表達顯著下降（P＜0.05、0.01）。結(jié)論 阿司匹林可通過上調(diào)E-cadherin蛋白的表達、抑制上皮間質(zhì)轉(zhuǎn)化進程從而抑制人鼻咽癌CNE-1、5-8F細胞遷移侵襲，同時下調(diào)PI3K、Akt、Vimentin、Snail蛋白的表達進而抑制CNE-1、5-8F細胞增殖、遷移和侵襲能力。

Objective To investigate the effect and mechanism of aspirin on the proliferation, migration and invasion of CNE-1 and 5-8F cells in human nasopharyngeal carcinoma. Methods Human nasopharyngeal carcinoma cell lines CNE-1 and 5-8F were divided into control group and aspirin (0.00, 1.25, 2.50, 5.00, and 10.00 mmol/L) treatment group. The proliferation capacity of CNE-1 and 5-8F cells was detected by MTT assay after the treatment of aspirin with different concentrations for 24, 48, and 72 h, IC₅₀ was determined as the concentration for subsequent experimental drug treatment. The proliferation ability of CNE-1 and 5-8F cells was detected by colony formation assay, and the migration and invasion ability of CNE-1 and 5-8F cells were detected by Transwell assay. The relative expression levels of Akt, PI3K, Vimentin, E-cadherin, and Snail in CNE-1 and 5-8F cells were detected by Western blotting. Results Human nasopharyngeal carcinoma CNE-1 and 5-8F cells were treated with 1.25, 2.50, 5.00, and 10.00 mmol/L aspirin, respectively, and the cell proliferation was inhibited in different degrees, which showed time and concentration correlation, and IC₅₀ were 3.3 and 2.7 mmol/L, respectively. After treatment with aspirin, the cell proliferation and colony formation ability of nasopharyngeal carcinoma CNE-1 and 5-8F cells were significantly decreased compared with the control group (P<0.01). Compared with the control group, the scratch healing rate in the aspirin treatment group was significantly decreased (P<0.05). Trasnwell migration assay showed that compared with the control group, the number of nasopharyngeal carcinoma cells CNE-1 and 5-8F passing through the compartment at 48 h in aspirin treatment group was significantly reduced (P<0.05, 0.001). Compared with the control group, the expression of E-cadherin in CNE-1 and 5-8F cells in aspirin treatment group was significantly increased (P<0.05), and the expression of PI3K, Akt, Vimentin and Snail was significantly decreased (P<0.05, 0.01). Conclusions Aspirin can inhibit the migration and invasion of human nasopharyngeal carcinoma CNE-1 and 5-8F cells by up-regulating the expression of E-cadherin protein and inhibiting the process of epithelial mesenchymal transformation, while down-regulating the expressions of PI3K, Akt, Vimentin and Snail proteins, thus inhibiting the proliferation, migration and invasion of CNE-1 and 5-8F cells.

R965

國家自然科學基金資助項目（81960172）；廣西自然科學基金資助項目（2020GXNSFAA238014）；桂林醫(yī)學院博士科研啟動項目（20501019035）