發(fā)布時(shí)間：2018-07-04 09:17

  本文選題：蛋白激酶抑制劑 + AT13148　； 參考：《華中科技大學(xué)》2016年博士論文

【摘要】：第一部分 蛋白激酶抑制劑AT13148對(duì)胃癌細(xì)胞生物學(xué)活性的影響目的：通過(guò)分組實(shí)驗(yàn)研究蛋白激酶抑制劑AT13148對(duì)不同類(lèi)型胃癌細(xì)胞增殖和凋亡的影響。對(duì)比分析不同濃度的蛋白激酶抑制劑AT13148與胃癌細(xì)胞凋亡的相關(guān)性。探索AT13148對(duì)胃癌細(xì)胞增殖的抑制作用是否通過(guò)促進(jìn)細(xì)胞凋亡來(lái)實(shí)現(xiàn)。方法：分別用不同濃度的蛋白激酶抑制劑AT13148 (0.1,1,5,10μmol/L)處理不同類(lèi)型的人胃癌細(xì)胞(包括HGC27、AGS、SNU-601、MKN-28、N87)和正常胃上皮細(xì)胞GEC-1,通過(guò)MTT, Brdu染色和臺(tái)盼藍(lán)染色分析蛋白激酶抑制劑AT13148處理后的胃癌細(xì)胞系各型細(xì)胞株的增殖能力,并通過(guò)TUNEL. Annexin V和caspase-3活性檢測(cè)試驗(yàn)來(lái)驗(yàn)證AT13148對(duì)胃癌細(xì)胞的抑制作用是否通過(guò)促進(jìn)細(xì)胞凋亡實(shí)現(xiàn)的。結(jié)果：不同濃度的蛋白激酶抑制劑AT13148 (0.1,1,5,10μmol/L)處理不同類(lèi)型的胃癌細(xì)胞后,MTT, Brdu染色和臺(tái)盼藍(lán)染色實(shí)驗(yàn)證明胃癌細(xì)胞系HGC27、AGS、SNU-601、MKN-28、N87和胃上皮細(xì)胞GEC-1的增殖能力與空白對(duì)照組相比均有不同程度地降低,且與作用時(shí)間呈正相關(guān),在48h之后的影響更為明顯,同時(shí)實(shí)驗(yàn)結(jié)果顯示AT13148抑制胃癌細(xì)胞增殖和促進(jìn)細(xì)胞死亡的作用呈濃度依賴(lài)性。TUNEL, Annexin V和caspase-3活性檢測(cè)試驗(yàn)顯示：AT13148處理胃癌HGC27細(xì)胞后,細(xì)胞凋亡數(shù)和caspase-3活性明顯增加；使用caspase和caspase-3抑制劑阻斷caspase-3途徑后,再用TUNEL, MTT和臺(tái)盼藍(lán)染色實(shí)驗(yàn)檢測(cè),結(jié)果顯示細(xì)胞凋亡和增殖指數(shù)都有所恢復(fù)。結(jié)論：蛋白激酶抑制劑AT13148能夠抑制胃癌細(xì)胞增殖并且促進(jìn)腫瘤細(xì)胞凋亡,其抑制細(xì)胞增殖和促進(jìn)凋亡的作用呈濃度依賴(lài)性。AT13148抑制胃癌細(xì)胞增殖的作用可以通過(guò)促進(jìn)腫瘤細(xì)胞凋亡來(lái)實(shí)現(xiàn)。第二部分AT13148通過(guò)PI3K/Akt信號(hào)通路調(diào)控胃癌細(xì)胞增殖及凋亡的作用機(jī)制目的：探索蛋白激酶抑制劑AT13148調(diào)控胃癌細(xì)胞增殖及凋亡作用的可能機(jī)制,通過(guò)實(shí)驗(yàn)來(lái)驗(yàn)證其是否通過(guò)PI3K/Akt信號(hào)通路來(lái)完成對(duì)胃癌細(xì)胞的調(diào)控作用。方法：分別用不同濃度的蛋白激酶抑制劑AT13148 (0.1,1,5,10μmol/L)處理胃癌細(xì)胞HGC27和AGS細(xì)胞1h并通過(guò)western blot方法測(cè)定PI3K/Akt信號(hào)通路中幾個(gè)重要的下游因子(比如Akt、GSK3β、p70S6K等相關(guān)激酶)的磷酸化水平和總的蛋白水平,并進(jìn)行相關(guān)性分析。結(jié)果：胃癌細(xì)胞HGC27和AGS細(xì)胞經(jīng)過(guò)不同濃度的AT13148 (0.1,1,5, 10μmol/L)處理后1h,測(cè)得Akt、GSK3β、p70S6K和RSK等激酶的磷酸化水平與空白對(duì)照組相比均有不同程度地降低,且有明顯的濃度依賴(lài)性,以10μmol/L的作用最為明顯,但是各組總的蛋白水平無(wú)明顯改變。結(jié)論：蛋白激酶抑制劑AT13148抑制胃癌細(xì)胞HGC27和AGS細(xì)胞的細(xì)胞增殖和促進(jìn)凋亡的作用是通過(guò)抑制PI3K/Akt信號(hào)通路中與生長(zhǎng)相關(guān)的蛋白激酶(比如Akt、GSK3β、p70S6K等)的活化來(lái)實(shí)現(xiàn)的。第三部分 蛋白激酶抑制劑AT13148對(duì)胃癌細(xì)胞裸鼠移植瘤的調(diào)控作用目的：建立裸鼠胃癌移植瘤模型,觀察無(wú)干預(yù)狀態(tài)下裸鼠移植瘤的生長(zhǎng),對(duì)比研究蛋白激酶抑制劑AT13148對(duì)胃癌細(xì)胞裸鼠移植瘤的調(diào)控作用。方法：用人胃癌細(xì)胞HGC27建立裸鼠移植瘤模型,選取30只造模成功的BALB/c-nu雌性裸鼠,隨機(jī)分為3組,每組10只。對(duì)照組10只每天經(jīng)口腔灌胃適量生理鹽水；A組10只每天按照15 mg/kg經(jīng)口腔灌胃AT13148；B組10只每天按照45 mg/kg經(jīng)口腔灌胃AT13148。開(kāi)始治療后每三天測(cè)定各組裸鼠移植瘤的成瘤體積以及荷瘤裸鼠的體重,三周后處死各組裸鼠,留取腫瘤組織標(biāo)本,用免疫印跡法(western blot)檢測(cè)移植瘤組織中Akt、GSK3β、p70S6K等蛋白激酶的表達(dá)及磷酸化水平；通過(guò)免疫組織化學(xué)實(shí)驗(yàn)檢測(cè)p-GSK3β在移植瘤瘤體中的表達(dá),并將三組數(shù)據(jù)進(jìn)行統(tǒng)計(jì)學(xué)分析比較。結(jié)果：成功建立人胃癌細(xì)胞HGC27裸鼠移植瘤模型。A、B兩組荷瘤裸鼠的移植瘤體積在各個(gè)時(shí)間點(diǎn)均明顯小于對(duì)照組移植瘤體積。三組荷瘤裸鼠體重?zé)o明顯差異。瘤體的Western blotting結(jié)果顯示A、B兩個(gè)實(shí)驗(yàn)組移植瘤組織中磷酸化水平均降低,且與AT13148的濃度呈負(fù)相關(guān)。免疫組化實(shí)驗(yàn)結(jié)果顯示p-GSK3β在AT13148處理后的裸鼠移植瘤組織中的表達(dá)較對(duì)照組明顯降低,表現(xiàn)為棕黃色顆粒減少。結(jié)論：蛋白激酶抑制劑AT13148可以抑制裸鼠體內(nèi)Akt、GSK3β、p70S6K等激酶的磷酸化,從而阻斷PI3K/Akt信號(hào)傳導(dǎo)通路過(guò)度活化,進(jìn)而發(fā)揮抑制腫瘤細(xì)胞惡性增殖的作用,但對(duì)裸鼠本身沒(méi)有藥物毒性。
[Abstract]:The effect of protein kinase inhibitor AT13148 on biological activity of gastric cancer cells in part 1: the effect of protein kinase inhibitor AT13148 on the proliferation and apoptosis of different types of gastric cancer cells was studied by grouping experiments. The correlation between AT13148 and apoptosis of gastric cancer cells was compared and analyzed, and AT13148 was explored. Whether the inhibitory effect of gastric cancer cell proliferation is achieved by promoting apoptosis. Methods: different types of human gastric cancer cells (including HGC27, AGS, SNU-601, MKN-28, N87) and normal gastric epithelial cells are treated with different concentrations of protein kinase inhibitor AT13148 (0.1,1,5,10 micron mol/L), and GEC-1 in normal gastric epithelial cells by MTT, Brdu staining and trypan blue. The proliferation ability of various cell lines of gastric cancer cell lines treated with protein kinase inhibitor AT13148 and the test of TUNEL. Annexin V and caspase-3 activity test to verify whether the inhibitory effect of AT13148 on gastric cancer cells is realized by promoting cell apoptosis. Results: AT13148 (0.1,1,5,10 u mol) of protein kinase inhibitor at different concentrations (0.1,1,5,10 u mol). /L) after the treatment of different types of gastric cancer cells, MTT, Brdu staining and trypan blue staining showed that the proliferation ability of gastric cancer cell lines HGC27, AGS, SNU-601, MKN-28, N87 and gastric epithelial cells decreased in varying degrees compared with the blank control group, and had a positive correlation with the action time, and the effect was more obvious after 48h, at the same time the experimental knot was found. The results showed that AT13148 inhibited the proliferation of gastric cancer cells and promoted cell death in a concentration dependent.TUNEL. The test of Annexin V and caspase-3 activity showed that the number of apoptosis and the activity of Caspase-3 increased significantly after AT13148 treatment of gastric cancer HGC27 cells, and the caspase-3 pathway was blocked by caspase and caspase-3 inhibitors. The results of TT and trypan blue staining showed that the apoptosis and proliferation index were all recovered. Conclusion: protein kinase inhibitor AT13148 can inhibit the proliferation of gastric cancer cells and promote the apoptosis of tumor cells. The inhibitory effect of.AT13148 on the proliferation of gastric cancer cells in a concentration dependent manner can inhibit the proliferation of gastric cancer cells. The second part AT13148 regulates the proliferation and apoptosis of gastric cancer cells through PI3K/Akt signaling pathway: explore the possible mechanism of protein kinase inhibitor AT13148 to regulate the proliferation and apoptosis of gastric cancer cells, and verify whether it completes the stomach through the PI3K/Akt signaling pathway. The regulation of cancer cells. Methods: the HGC27 and AGS cells 1h of gastric cancer cells were treated with different concentration of protein kinase inhibitor AT13148 (0.1,1,5,10 mol/L), and the phosphorylation level and total protein of several important downstream factors (Akt, GSK3 beta, p70S6K and other related kinases) in the PI3K/Akt signaling pathway were measured by Western blot method. Results: the HGC27 and AGS cells of gastric cancer cells were treated with different concentrations of AT13148 (0.1,1,5, 10 mu mol/L) after 1h. The phosphorylation levels of Akt, GSK3 beta, p70S6K and RSK were decreased in varying degrees compared with those of the blank control group, with a significant concentration dependence, and the most important effect was 10 mu mol/L. Obviously, the total protein level of each group was not significantly changed. Conclusion: the inhibitory effect of protein kinase inhibitor AT13148 on the proliferation and apoptosis of gastric cancer cells HGC27 and AGS cells is achieved by inhibiting the activation of the growth related protein kinase (such as Akt, GSK3 beta, p70S6K, etc.) in the PI3K/Akt signaling pathway. The third part of the egg Regulatory effect of white kinase inhibitor AT13148 on xenografts in nude mice of gastric cancer cells: to establish a nude mouse model of gastric cancer transplantation, to observe the growth of xenografts in nude mice without intervention, and to compare the regulatory effect of protein kinase inhibitor AT13148 on xenografts in nude mice of gastric cancer cells: a nude mouse transplantation with human gastric cancer cell HGC27 30 BALB/c-nu female nude mice were randomly divided into 3 groups, 10 in each group, 10 in the control group, and 10 in the oral administration of normal saline every day in the oral cavity, and 10 in the A group by 15 mg/kg by the oral gavage of the stomach every day; 10 in the B group were treated with the oral gavage of the stomach by the mouth of 45 mg/kg every day for the treatment of nude mice every three days. The tumor volume and the weight of the tumor bearing nude mice were killed three weeks after the tumor tissue specimens were left. The expression of Akt, GSK3 beta, p70S6K and other protein kinase in the transplanted tumor tissues were detected by immunoblotting (Western blot). The expression of p-GSK3 beta in the transplanted tumor was detected by immunohistochemistry and the expression of p-GSK3 beta in the tumor transplanted tumor was detected. Three groups of data were compared statistically. Results: human gastric cancer cell HGC27 nude mice transplanted tumor model.A was successfully established. The volume of transplanted tumor in B two group of nude mice was significantly smaller than that of the control group. There was no significant difference between the three groups of tumor bearing nude mice. The Western blotting results of the tumor showed A, B and the two experimental groups. The level of phosphorylation in the tumor tissue decreased and was negatively correlated with the concentration of AT13148. The immunohistochemical results showed that the expression of p-GSK3 beta in the transplanted tumor tissues of nude mice after AT13148 treatment was significantly lower than that of the control group, showing a decrease in brown granules. Conclusion: protein kinase inhibitor AT13148 can inhibit Akt, GSK3 beta, p70 in nude mice. The phosphorylation of S6K and other kinases, thus blocking the excessive activation of the PI3K/Akt signal transduction pathway, thus inhibits the malignant proliferation of tumor cells, but has no drug toxicity to nude mice.
【學(xué)位授予單位】：華中科技大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2016
【分類(lèi)號(hào)】：R735.2

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2 衣曉峰　喬蕤琳 記者 趙宇清;抑制胃癌細(xì)胞生長(zhǎng)研究有新發(fā)現(xiàn)[N];黑龍江日?qǐng)?bào);2010年

3 記者 衣曉峰　通訊員 喬蕤琳;維生素E衍生物能抑制胃癌細(xì)胞生長(zhǎng)[N];健康報(bào);2010年

4 王振嶺;我國(guó)抑制胃癌細(xì)胞生長(zhǎng)研究有重要發(fā)現(xiàn)[N];中國(guó)醫(yī)藥報(bào);2002年

5 王振嶺;抗癌藥抑制胃癌細(xì)胞生長(zhǎng)研究獲重要發(fā)現(xiàn)[N];中國(guó)中醫(yī)藥報(bào);2002年

6 王振嶺;7種抗癌藥體外抑制胃癌細(xì)胞的研究有新發(fā)現(xiàn)[N];醫(yī)藥經(jīng)濟(jì)報(bào);2002年

7 張中橋;胃癌細(xì)胞MDR機(jī)制研究取得新進(jìn)展[N];中國(guó)醫(yī)藥報(bào);2007年

8 吳一福 蘇玉軍;白藜蘆醇可誘導(dǎo)胃癌細(xì)胞脫落凋亡[N];中國(guó)醫(yī)藥報(bào);2005年

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1 李雙玲;IGF-1通過(guò)抑制Fox01核保留促進(jìn)胃癌細(xì)胞生長(zhǎng)機(jī)制的研究[D];山東大學(xué);2015年

2 胡偉國(guó);腫瘤相關(guān)成纖維細(xì)胞中Thy-1激活誘導(dǎo)上皮間質(zhì)轉(zhuǎn)化促進(jìn)胃癌細(xì)胞侵襲轉(zhuǎn)移的研究[D];上海交通大學(xué);2014年

3 周韻斕;應(yīng)激條件下胃癌細(xì)胞高表達(dá)線粒體活性氧和前梯度蛋白2促進(jìn)腫瘤進(jìn)展的研究[D];上海交通大學(xué);2014年

4 徐同鵬;SP1誘導(dǎo)的長(zhǎng)非編碼RNA TINCR通過(guò)調(diào)控KLF2 mRNA穩(wěn)定性影響胃癌細(xì)胞的增殖與凋亡[D];南京醫(yī)科大學(xué);2015年

5 王暢;miR-34a通過(guò)miR-34a-c-myc/Bmi-1負(fù)反饋通路負(fù)調(diào)控胃癌干細(xì)胞樣特性[D];復(fù)旦大學(xué);2014年

6 羅貫虹;MGr1-Ag/37LRP參與PrP~C介導(dǎo)的胃癌細(xì)胞多藥耐藥[D];第四軍醫(yī)大學(xué);2014年

7 默董亮;人類(lèi)解旋酶RecQL4調(diào)控胃癌細(xì)胞耐藥性分子機(jī)制研究[D];中國(guó)科學(xué)院北京基因組研究所;2016年

8 劉皎婧;PI3K/Akt/GSK3β/p190ARhoGAP/RhoA信號(hào)通路在Wnt5a誘導(dǎo)胃癌細(xì)胞遷移中作用的研究[D];南京醫(yī)科大學(xué);2014年

9 Muhammad Kamran（卡姆拉）;[D];大連醫(yī)科大學(xué);2015年

10 王瑛;PKGⅡ?qū)PA誘導(dǎo)的胃癌細(xì)胞徖移及RhoA和Rac1激活的影響[D];江蘇大學(xué);2015年

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1 林光錟;CyclinA/CDK2介導(dǎo)BAG3 Ser291位點(diǎn)的磷酸化并影響胃癌細(xì)胞的增殖和凋亡[D];福建醫(yī)科大學(xué);2015年

2 蔡洙哲;p12-LOX對(duì)胃癌細(xì)胞MKN-28的增殖和遷移的影響[D];延邊大學(xué);2015年

3 李龍;Her-2高表達(dá)對(duì)胃癌細(xì)胞侵襲、遷移的影響[D];長(zhǎng)江大學(xué);2015年

4 趙婷婷;GPIbα對(duì)胃癌細(xì)胞粘附、遷移和侵襲能力的影響及其機(jī)制的初步探討[D];蘭州大學(xué);2015年

5 謝瑞霞;盤(pán)狀結(jié)構(gòu)域受體1調(diào)控上皮—間質(zhì)轉(zhuǎn)化影響胃癌侵襲轉(zhuǎn)移分子機(jī)制的研究[D];蘭州大學(xué);2015年

6 王東倉(cāng);NM23-H2通過(guò)抑制Wnt/β-catenin信號(hào)通路抑制胃癌細(xì)胞的侵襲遷移[D];蘭州大學(xué);2015年

7 朱瑞雪;NDRG2基因?qū)ξ赴┘?xì)胞惡性表型的影響[D];鄭州大學(xué);2015年

8 董凱楠;內(nèi)質(zhì)網(wǎng)應(yīng)激對(duì)胃癌細(xì)胞侵襲遷移能力的影響[D];鄭州大學(xué);2015年

9 單爭(zhēng)爭(zhēng);二甲雙胍在IL-6誘導(dǎo)胃癌細(xì)胞EMT中的作用[D];鄭州大學(xué);2015年

10 田莉;NM23-H2通過(guò)誘導(dǎo)自噬抑制胃癌細(xì)胞EMT的發(fā)生[D];蘭州大學(xué);2015年

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