本文選題：高遷移率族蛋白 + 膀胱癌細胞�。� 參考：《中國腫瘤生物治療雜志》2017年03期

【摘要】：目的:探討高遷移率族蛋白1(high-mobility group box 1,HMGB1)對膀胱癌T24株細胞的增殖、凋亡及惡性生物學(xué)行為的影響及其潛在作用機制。方法:收集2014年12月至2016年1月期間重慶醫(yī)科大學(xué)附屬第一醫(yī)院泌尿外科病區(qū)手術(shù)切除的20例膀胱癌以及相應(yīng)癌旁組織,免疫組化方法檢測膀胱癌和癌旁組織HMGB1表達差異;應(yīng)用RNAi處理T24細胞并分為空白對照組(Blank)、陰性對照組(NC)和干擾組(si HMGB1);CCK-8、流式細胞術(shù)、劃痕實驗和Transwell侵襲實驗分別檢測HMGB1敲低后對T24細胞增殖、凋亡、周期、遷移以及侵襲能力的影響;Western blotting檢測不同膀胱癌細胞株BIU-87和T24細胞的HMGB1表達水平以及敲低HMGB1對T24細胞惡性生物學(xué)行為相關(guān)蛋白的影響。結(jié)果:與癌旁組織相比,HMGB1在膀胱癌組織處于高表達狀態(tài)[(67.33±4.91)vs(12.00±3.79),P0.05]。與NC組和Blank組相比,si HMGB1組細胞增殖受抑制(P0.05);流式細胞術(shù)提示敲低HMGB1后細胞凋亡率增加,細胞周期阻滯在G0/G1期;劃痕實驗及Transwell侵襲實驗顯示,敲低HMGB1后細胞遷移(P0.05)以及侵襲[穿膜細胞數(shù):(16.33±1.45)vs(35.00±1.53)、(34.00±2.08)個,均P0.05]能力減弱;Western blotting結(jié)果顯示敲低后E-鈣黏著蛋白表達上調(diào)(P0.05),N-鈣黏著蛋白、波形蛋白、基質(zhì)金屬蛋白酶(metrix metalloproteinase,MMP)-2、MMP-9、細胞周期蛋白D1、c-Myc、β-聯(lián)蛋白表達下調(diào)(均P0.05)。結(jié)論:HMGB1可通過促進膀胱癌細胞EMT進而增強其惡性生物學(xué)行為,其機制可能是通過β-聯(lián)蛋白信號通路介導(dǎo)。
[Abstract]:Objective: to investigate the effects of high mobility group protein 1(high-mobility group box 1 HMGB1 on the proliferation, apoptosis and malignant biological behavior of bladder cancer cell line T24. Methods: from December 2014 to January 2016, 20 cases of bladder cancer and its adjacent tissues were collected from the urology ward of the first affiliated Hospital of Chongqing Medical University. The expression of HMGB1 in bladder cancer and adjacent tissues was detected by immunohistochemical method. T24 cells were treated with RNAi and divided into blank control group, negative control group and interference group. Flow cytometry, scratch test and Transwell invasion assay were used to detect the proliferation, apoptosis and cycle of T24 cells after HMGB1 knockout. The expression of HMGB1 in different bladder cancer cell lines BIU-87 and T24 cells was detected by Western blotting and the effect of knock down HMGB1 on the expression of proteins associated with malignant biological behavior of T24 cells was evaluated by Western blotting. Results: the expression of HMGB1 in bladder cancer tissues was higher than that in paracancerous tissues [67.33 鹵4.91)vs(12.00 鹵3.79 P 0.05]. Compared with NC group and Blank group, cell proliferation was inhibited in HMGB1 group (P 0.05), apoptosis rate was increased and cell cycle was blocked in G0/G1 phase after knockdown with low HMGB1 by flow cytometry. The ability of cell migration (P0.05) and invasion (16.33 鹵1.45)vs(35.00 鹵1.53 鹵34.00 鹵2.08) of cell migration after knockdown (P0.05) was decreased. The results of Western blotting showed that the expression of E-cadherin up-regulated the expression of P0.05 N-cadherin and vimentin after knockout. The expression of matrix metalloproteinase (MMP), MMP- 2, MMP-9, and cyclin D1, c-Myc, 尾-binding protein were down-regulated (all P 0.05). ConclusionHMGB1 can enhance the malignant biological behavior of bladder cancer cells by promoting EMT, and its mechanism may be mediated by 尾 -integrin signaling pathway.
【作者單位】： 重慶醫(yī)科大學(xué)附屬第一醫(yī)院泌尿外科;重慶醫(yī)科大學(xué)附屬第一醫(yī)院重慶市分子腫瘤及表觀遺傳學(xué)重點實驗室;
【基金】：國家自然科學(xué)基金資助項目(No.81372758)~~
【分類號】：R737.14

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