本文關(guān)鍵詞： 重組人程序性細(xì)胞死亡蛋白 子宮內(nèi)膜癌 紫杉醇 耐藥性 敏感性　出處：《中國腫瘤生物治療雜志》2017年10期 　論文類型：期刊論文

【摘要】：目的:探討在子宮內(nèi)膜癌細(xì)胞中重組人程序性細(xì)胞死亡蛋白5(recombinant human programmed cell death protein 5,rhPDCD5)對紫杉醇化療的促進(jìn)作用。方法:子宮內(nèi)膜癌KLE細(xì)胞培養(yǎng)完成后,通過重組人rh PDCD5(20μg/ml)處理KLE細(xì)胞,再分別以0、1.0、5.0、10.0、50μmol/L紫杉醇(paclitaxel,PTX)處理24 h或以10μmol/L PTX處理0、12、24、48 h,提取細(xì)胞總RNA及蛋白后,CCK法檢測KLE細(xì)胞的增殖情況,流式細(xì)胞術(shù)檢測KLE細(xì)胞凋亡情況,實(shí)時(shí)定量PCR檢測KLE細(xì)胞中PDCD5mRNA的表達(dá)量,實(shí)時(shí)定量PCR或Western blotting測定凋亡相關(guān)基因的Bax、Bcl2、caspase-3 mRNA或蛋白水平的變化。結(jié)果:PTX對PDCD5表達(dá)的促進(jìn)作用具有劑量依賴性和時(shí)間依賴性;PTX的最佳作用濃度為10μmol/L,最佳作用時(shí)間為24 h。rh PDCD5明顯增強(qiáng)紫杉醇對KLE細(xì)胞的抑制作用。CCK實(shí)驗(yàn)、流式細(xì)胞術(shù)及Western blotting檢測顯示:PTX+rhPDCD5聯(lián)合處理組KLE細(xì)胞的增殖抑制率和凋亡率均較PTX組明顯增加、pro-caspase 3的表達(dá)量明顯增加(均P0.01)。促進(jìn)凋亡蛋白Bax和抑制凋亡蛋白Bcl2的比值亦較明顯增加(P0.01)。結(jié)論:rhPDCD5可協(xié)同PTX抑制子宮內(nèi)膜癌KLE細(xì)胞的增殖、促進(jìn)細(xì)胞的凋亡,可明顯增強(qiáng)KLE細(xì)胞對PTX的藥物敏感性。
[Abstract]:Objective: to investigate the effect of recombinant human programmed cell death protein 5 (rhPDCD5) on paclitaxel chemotherapy in endometrial cancer cells. Methods: KLE cells were treated with recombinant human rhPDCD5 20 渭 g / ml after the completion of KLE cell culture. The cell total RNA and protein were extracted for 24 h or 10 渭 mol/L PTX for 24 h, respectively. The proliferation of KLE cells was detected by flow cytometry. The apoptosis of KLE cells was detected by flow cytometry, and the expression of PDCD5mRNA in KLE cells was detected by real time quantitative PCR. Real time quantitative PCR or Western blotting was used to detect the changes of Baxia Bcl2 caspase-3 mRNA or protein in apoptosis-related genes. Results the optimal concentration of PDCD5 expression was 10 渭 mol / L and the optimal time was 10 渭 mol / L for the promotion of PDCD5 expression by 1: PTX in a dose and time dependent manner. The inhibitory effect of paclitaxel on KLE cells was significantly enhanced by 24 h. Rh PDCD5. The results of flow cytometry and Western blotting analysis showed that the proliferation inhibition rate and apoptosis rate of KLE cells treated with WPTX rhPDCD5 were significantly higher than those of PTX group (all P 0.01). The ratio of Bax to Bcl2 was significantly higher than that of PTX group. Conclusion: rhPDCD5 can inhibit the proliferation of endometrial carcinoma KLE cells in combination with PTX. The drug sensitivity of KLE cells to PTX was significantly enhanced by promoting cell apoptosis.
【作者單位】： 重慶市中醫(yī)院腫瘤科;
【分類號】：R737.33

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