本文選題：前列腺癌 + 羧基末端結(jié)合蛋白2　； 參考：《天津醫(yī)科大學(xué)》2016年博士論文

【摘要】：目的:本研究通過shRNA干擾技術(shù)建立穩(wěn)定低表達(dá)CtBP2的前列癌C4-2細(xì)胞,利用體內(nèi)外實(shí)驗(yàn)技術(shù)檢測CtBP2低表達(dá)對C4-2細(xì)胞增殖、凋亡及遷移侵襲能力的影響;并揭示CtBP2調(diào)控C4-2細(xì)胞上述生物學(xué)行為的具體機(jī)制。為未來臨床靶向CtBP2基因治療前列腺癌提供理論基礎(chǔ)。方法:1.通過實(shí)時(shí)熒光定量聚合酶鏈反應(yīng)(RT-qPCR)檢測前列腺癌組織和癌旁組織中Ctbp2 mRNA表達(dá)量;通過免疫組化檢測前列腺癌組織和癌旁組織中Ctbp2蛋白的表達(dá)水平;將靶向Ctbp2基因shRNA質(zhì)粒及陰性對照(Vector)質(zhì)粒分別轉(zhuǎn)入C4-2細(xì)胞,RT-qPCR和western blot法分別檢測Ctbp2 mRNA及蛋白的表達(dá)水平以檢驗(yàn)治療轉(zhuǎn)染的效率;細(xì)胞計(jì)數(shù)試劑盒(CCK-8)法和流式細(xì)胞儀分別檢測下調(diào)Ctbp2表達(dá)對C4-2細(xì)胞體外增殖能力和凋亡的影響;裸鼠皮下移植瘤實(shí)驗(yàn)觀察下調(diào)Ctbp2對C4-2細(xì)胞體內(nèi)成瘤能力的影響;利用Ctbp2特異性底物MTOB暴露C4-2細(xì)胞檢測其對C4-2細(xì)胞增殖能力的影響,以此進(jìn)一步驗(yàn)證Ctbp2表達(dá)對C4-2細(xì)胞體外增殖能力的影響;通過western blot實(shí)驗(yàn)檢測下調(diào)Ctbp2表達(dá)水平對凋亡相關(guān)蛋白BIK表達(dá)水平的影響。2、通過Transwell實(shí)驗(yàn)檢測下調(diào)Ctbp2對C4-2細(xì)胞體外侵襲(預(yù)鋪膠)和遷移能力的影響;通過建立裸鼠皮下移植瘤,在細(xì)胞移植后第45天時(shí)利用小動(dòng)物活體成像儀檢測腫瘤細(xì)胞在胸腹腔臟器和骨骼等部位有無轉(zhuǎn)移灶;通過RT-qPCR檢測下調(diào)Ctbp2對C4-2細(xì)胞上皮標(biāo)志分子E-cadherin mRNA表達(dá)水平的影響;通過western blot實(shí)驗(yàn)檢測下調(diào)Ctbp2對C4-2細(xì)胞上皮標(biāo)志分子E-cadherin和間質(zhì)標(biāo)志分子N-cadherin蛋白表達(dá)水平的影響;通過鬼筆環(huán)肽染色細(xì)胞骨架檢測下調(diào)Ctbp2對C4-2細(xì)胞細(xì)胞骨架結(jié)構(gòu)的影響;通過分析UCSC數(shù)據(jù)庫中的信息,搜尋關(guān)于Ctbp2與RhoC之間存在相互作用關(guān)系的證據(jù);通過RT-qPCR檢測下調(diào)Ctbp2對C4-2細(xì)胞上皮標(biāo)志分子RhoC mRNA表達(dá)水平的影響;通過western blot實(shí)驗(yàn)檢測下調(diào)Ctbp2對C4-2細(xì)胞中RhoC-ROCK1-MLC信號通路中蛋白表達(dá)水平的影響。結(jié)果:1.Ctbp2 mRNA在前列腺癌組織中的表達(dá)水平顯著高于癌旁正常組織(2.79±1.04比1.0±0.41)(p0.05);ctbp2蛋白質(zhì)表達(dá)水平在前列腺癌組織中也較癌旁組織中顯著增高;通過ctbp2-shrna轉(zhuǎn)染c4-2細(xì)胞可顯著降低細(xì)胞中ctbp2mrna和蛋白的表達(dá)水平;通過cck-8試劑盒檢測穩(wěn)定低表達(dá)ctbp2基因的c4-2細(xì)胞24小時(shí)內(nèi)的增殖能力,發(fā)現(xiàn)降低ctbp2的表達(dá)水平可顯著減弱c4-2細(xì)胞的增殖能力(0.59±0.11)(p0.05),而vector組細(xì)胞(0.58±0.09)的增殖能力與cont組c4-2細(xì)胞(0.34±0.05)間無顯著差異,(p0.05);細(xì)胞克隆形成實(shí)驗(yàn)發(fā)現(xiàn)降低ctbp2的表達(dá)水平可顯著減弱c4-2細(xì)胞的克隆形成能力;通過不同濃度mtob暴露c4-2細(xì)胞檢測其對c4-2細(xì)胞增殖能力的影響,結(jié)果顯示c4-2細(xì)胞增殖能力隨著mtob濃度(0.1mm、0.5mm、1mm、4mm、7mm、10mm)的增加而逐漸降低(0.102±0.013,0.104±0.014,0.097±0.006,0.086±0.004,0.063±0.007,0.034±0.004,0.023±0.004);通過裸鼠皮下移植瘤實(shí)驗(yàn)發(fā)現(xiàn),降低ctbp2的表達(dá)水平可顯著減弱c4-2細(xì)胞在小鼠體內(nèi)的增殖能力,細(xì)胞皮下移植后第35天ctbp2組和vector組小鼠的腫瘤體積分別為893.28±241.15mm3vs2173.83±472.71mm3(p0.05);通過annexinv-pi染色,利用流式細(xì)胞儀檢測細(xì)胞的凋亡情況,結(jié)果發(fā)現(xiàn)下調(diào)ctbp2的表達(dá)水平可顯著促進(jìn)c4-2細(xì)胞的凋亡cont組ctbp2-shrna組凋亡細(xì)胞數(shù)量分別為10.10%±0.96%vs41.00%±3.01%(p0.05),而vector組和cont組之間無顯著差異,(p0.05);通過westernblot實(shí)驗(yàn)發(fā)現(xiàn)降低ctbp2的表達(dá)水平可顯著促進(jìn)c4-2細(xì)胞中凋亡相關(guān)蛋白bik的表達(dá)水平。2.transwell實(shí)驗(yàn)檢測降低ctbp2的表達(dá)水平對c4-2細(xì)胞的侵襲(預(yù)鋪膠)和遷移能力發(fā)現(xiàn),與cont組細(xì)胞相比較ctbp2-shrna組細(xì)胞的侵襲(63.25±6.75vs249.00±20.50)和遷移(805.50±63.25vs1639.25±71.38)能力均顯著被抑制(p0.05),而vector組和cont組間無顯著差異(p0.05);通過建立了皮下移植瘤裸鼠模型,并在細(xì)胞皮下移植后第45天時(shí)用小動(dòng)物活體成像儀檢測荷瘤小鼠體內(nèi)轉(zhuǎn)移灶的情況發(fā)現(xiàn)在10只vector組小鼠模型中檢測到有3只鼠發(fā)生了不同程度的腹部臟器轉(zhuǎn)移(主要為胃腸道系統(tǒng)),而在ctbp2-shrna組小鼠中未發(fā)現(xiàn)有腹部臟器轉(zhuǎn)移灶;另外在vector組有4只小鼠發(fā)生了骨轉(zhuǎn)移,轉(zhuǎn)移部位主要集中在四肢,而ctbp2-shrna組小鼠中未發(fā)現(xiàn)有骨轉(zhuǎn)移灶情況的發(fā)生。通過rt-qpcr和westernblot實(shí)驗(yàn)發(fā)現(xiàn)降低c4-2細(xì)胞中ctbp2的表達(dá)水平可顯著增強(qiáng)上皮細(xì)胞分子標(biāo)志物e-cadherinmrna和蛋白的表達(dá)水平,同時(shí)n-cadherin蛋白表達(dá)量下降;co-ip實(shí)驗(yàn)證實(shí)在c4-2細(xì)胞中ctbp2與e-cadherin轉(zhuǎn)錄因子slμg之間存在相互結(jié)合作用關(guān)系;通過鬼筆環(huán)肽染色細(xì)胞骨架發(fā)現(xiàn),降低C4-2細(xì)胞中CtBP2的表達(dá)水平可顯著減少細(xì)胞骨架成份;檢索UCSC數(shù)據(jù)庫得知CtBP2可結(jié)合在Rho C的啟動(dòng)子序列上,發(fā)揮轉(zhuǎn)錄因子的作用;通過RT-qPCR發(fā)現(xiàn)降低CtBP2的表達(dá)水平可使C4-2細(xì)胞中RhoC mRNA的表達(dá)量顯著下降,同時(shí)通過western blot實(shí)驗(yàn)發(fā)現(xiàn)RhoC下游信號分子ROCK1和p-MLC的蛋白表達(dá)量也下降。結(jié)論:1.輔助轉(zhuǎn)錄因子CtBP2在前列腺癌組織中高表達(dá);2.降低CtBP2的表達(dá)水平可顯著抑制前列腺癌C4-2細(xì)胞的體內(nèi)外增殖能力并促進(jìn)其凋亡;3.降低CtBP2的表達(dá)水平可顯著抑制前列腺癌C4-2細(xì)胞的體內(nèi)外侵襲遷移能力,且在體外CtBP2可通過EMT通路和RhoC-ROCK1通路調(diào)控C4-2細(xì)胞的侵襲遷移能力。
[Abstract]:Objective: to establish a prostex cancer C4-2 cell with low expression of CtBP2 by shRNA interference technique, and to detect the effect of CtBP2 low expression on the proliferation, apoptosis and migration and invasion of C4-2 cells in vivo and in vitro, and to reveal the specific mechanism of CtBP2 regulating the biological behavior of C4-2 cells in the future, and for the future clinical targeting of CtBP2 gene therapy. The theoretical basis of prostate cancer is provided. Methods: 1. the expression of Ctbp2 mRNA in prostate cancer tissue and para cancer tissue was detected by real-time quantitative polymerase chain reaction (RT-qPCR), and the expression of Ctbp2 protein in prostate cancer tissue and para cancer tissue was detected by immunohistochemistry; the target Ctbp2 gene shRNA plasmid and negative control (Vector) substance were targeted. The expression level of Ctbp2 mRNA and protein was detected by RT-qPCR and Western blot, respectively, to test the efficiency of transfection, respectively. Cell count Kit (CCK-8) and flow cytometry were used to detect the effect of down regulated Ctbp2 expression on the proliferation and apoptosis of C4-2 cells in vitro, and to observe the down-regulation of Ctbp in nude mice by subcutaneous transplantation of nude mice. 2 Effect on the tumor formation ability of C4-2 cells in vivo; the effect of C4-2 cells on the proliferation ability of C4-2 cells by Ctbp2 specific substrate MTOB was detected to further verify the effect of Ctbp2 expression on the proliferation ability of C4-2 cells in vitro; the BIK expression level of down regulated Ctbp2 tables was detected by Western blot test. The effect of.2 was detected by Transwell test. The effect of down-regulation of Ctbp2 on the invasion (pre paving) and migration ability of C4-2 cells in vitro was detected. By establishing subcutaneous transplanted tumor in nude mice, the tumor cells were detected by the small animal living imager at forty-fifth days after the transplantation, and the tumor cells were detected in the thoracic and abdominal organs and the bone and other parts of the bone, and the Ctb was down regulated by RT-qPCR. The effect of P2 on the expression level of C4-2 cell epithelial marker molecule E-cadherin mRNA; the effect of down regulated Ctbp2 on the expression of E-cadherin and interstitial marker molecule N-cadherin protein expression level of C4-2 cell epithelial marker molecules by Western blot test; the cytoskeleton structure of C4-2 cells was detected by cytoskeleton through the cytoskeleton of phallus cytosin staining. Influence; through the analysis of the information in the UCSC database, search for evidence about the interaction between Ctbp2 and RhoC, and the effect of Ctbp2 on the expression level of RhoC mRNA of the C4-2 cell epithelial markers by RT-qPCR detection; and the expression of protein expression in the signaling pathway in the C4-2 cells by Western blot experiment Results: the expression level of 1.Ctbp2 mRNA in prostate cancer tissues was significantly higher than that of normal tissue adjacent to the carcinoma (2.79 + 1.04 to 1 + 0.41) (P0.05), and the expression level of ctbp2 protein was significantly higher in the prostate cancer tissue than in the para cancerous tissue, and the ctbp2mrna and protein in the cells could be significantly reduced by ctbp2-shrna transfer to C4-2 cells. The proliferation ability of C4-2 cells with stable low expression of ctbp2 gene in 24 hours was detected by CCK-8 kit, and it was found that the expression level of ctbp2 decreased significantly (0.59 + 0.11) (P0.05), while there was no significant difference between the proliferation ability of vector group (0.58 + 0.09) and C4-2 cells (0.34 + 0.05) in cont group (P0.05). The cell clone formation experiment found that reducing the expression level of ctbp2 could significantly weaken the cloning and formation ability of C4-2 cells, and the effect on the proliferation ability of C4-2 cells was detected by C4-2 cells exposed to different concentrations of mtob. The results showed that the proliferation ability of C4-2 cells gradually decreased with the increase of mtob concentration (0.1mm, 0.5mm, 1mm, 4mm, 7mm, and 7mm). 0.013,0.104 + 0.014,0.097 + 0.006,0.086 + 0.004,0.063 + 0.007,0.034 + 0.004,0.023 + 0.004). By subcutaneous transplantation of nude mice, it was found that reducing the expression level of ctbp2 could significantly reduce the proliferation ability of C4-2 cells in mice, and the volume of tumor in ctbp2 group and vector group was 893.28 + 241.1 after thirty-fifth days after subcutaneous transplantation. 5mm3vs2173.83 + 472.71mm3 (P0.05); the apoptotic cells were detected by flow cytometry with annexinv-pi staining. The results showed that the number of apoptotic cells in the cont group of C4-2 cells was 10.10% + 0.96%vs41.00% + 3.01% (P0.05), respectively, and there was no significant difference between the vector group and the cont group. The difference, (P0.05); through the Westernblot experiment, it was found that reducing the expression level of ctbp2 significantly promoted the expression level of apoptosis related protein bik in C4-2 cells,.2.transwell test reduced the invasion (pre paving) and migration of C4-2 cells by ctbp2 expression level, and compared the invasion of the ctbp2-shrna group with the cont group cells (63.25 The ability of + 6.75vs249.00 + 20.50) and migration (805.50 + 63.25vs1639.25 + 71.38) were significantly inhibited (P0.05), but there was no significant difference between group vector and cont group (P0.05). A nude mouse model of subcutaneous transplantation tumor was established and the metastasis of tumor bearing mice was detected by small animal living imaging instrument at forty-fifth days after subcutaneous transplantation. In 10 vector mice, 3 rats were detected in different degrees of abdominal organ transfer (mainly the gastrointestinal tract), but no abdominal organ metastasis was found in group ctbp2-shrna mice; and 4 mice in group vector had bone metastases, and the metastatic sites were mainly concentrated on the limbs, while in group ctbp2-shrna mice were not found. RT-qPCR and Westernblot experiments showed that the expression level of ctbp2 in C4-2 cells decreased significantly, and the expression level of e-cadherinmrna and protein in the epithelial cell markers was significantly enhanced, while the expression of N-cadherin protein was decreased, and co-Ip experiments confirmed ctbp2 and E-cadherin transcription factor SL g in C4-2 cells. There is a binding relationship between the C4-2 cells and the cytoskeleton through the cytoskeleton. The reduction of the CtBP2 expression level in the C4-2 cells can significantly reduce the cytoskeleton component; the retrieval of the UCSC database shows that CtBP2 can be used in the promoter sequence of Rho C, and the expression level of CtBP2 can be reduced by RT-qPCR. The expression of RhoC mRNA in C4-2 cells decreased significantly, and the protein expression of ROCK1 and p-MLC in the downstream signal molecules of RhoC decreased by Western blot. Conclusion: the 1. auxiliary transcription factor CtBP2 is highly expressed in the prostate cancer tissue, and 2. to reduce the expression level of CtBP2 can significantly inhibit the proliferation of prostate cancer C4-2 cells in vivo and in vitro 3. reduced CtBP2 expression level significantly inhibited the invasion and migration of C4-2 cells in vitro and in vitro, and in vitro CtBP2 could regulate the invasion and migration of C4-2 cells through the EMT pathway and the RhoC-ROCK1 pathway.
【學(xué)位授予單位】：天津醫(yī)科大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：R737.25

【相似文獻(xiàn)】

相關(guān)期刊論文 前10條

1 張玉勤;;細(xì)胞分化再活化治療腫瘤[J];國外醫(yī)學(xué)情報(bào);1991年01期

2 David　Tenenbaum,饒新華;細(xì)胞之源[J];世界科學(xué);2000年11期

3 閆貴新;干細(xì)胞研究的重大進(jìn)展[J];畜牧獸醫(yī)科技信息;2000年11期

4 趙志力;付小兵;;正常與異常的細(xì)胞分化[J];感染.炎癥.修復(fù);2001年03期

5 趙志力;付小兵;;修復(fù)細(xì)胞分化的調(diào)控機(jī)制與鑒別[J];感染.炎癥.修復(fù);2001年04期

6 趙志力;修復(fù)細(xì)胞分化的調(diào)控機(jī)制與鑒別[J];中國危重病急救醫(yī)學(xué);2002年02期

7 趙志力;付小兵;;不同發(fā)育階段細(xì)胞的分化與調(diào)控機(jī)制[J];感染.炎癥.修復(fù);2002年01期

8 戴新貴;姚詠明;艾宇航;;輔助性T細(xì)胞17的研究進(jìn)展[J];生理科學(xué)進(jìn)展;2008年04期

9 ;細(xì)胞分化:一個(gè)兩階段的過程[J];中華婦幼臨床醫(yī)學(xué)雜志;2009年02期

10 黃紹勤;曹惠珍;;生命的基本單位——細(xì)胞[J];廣醫(yī)通訊;1980年03期

相關(guān)會(huì)議論文 前10條

1 徐志彥;;《細(xì)胞分化》教學(xué)案例(教學(xué)內(nèi)容安排1課時(shí))[A];河北省教師教育學(xué)會(huì)第二屆中小學(xué)教師教學(xué)案例展論文集[C];2013年

2 尹青;張雷;李莉;謝丹丹;龔淼;;體外心肌樣環(huán)境對P19細(xì)胞向心肌細(xì)胞分化的誘導(dǎo)作用[A];中國解剖學(xué)會(huì)2012年年會(huì)論文文摘匯編[C];2012年

3 丁建東;;圖案化表面與干細(xì)胞分化[A];2013年全國高分子學(xué)術(shù)論文報(bào)告會(huì)論文摘要集——大會(huì)邀請報(bào)告[C];2013年

4 陳思;黃欣;陳少華;楊力建;鄭海濤;李揚(yáng)秋;;BCL11B基因在T細(xì)胞分化和增殖中調(diào)節(jié)作用的研究[A];中國病理生理學(xué)會(huì)第九屆全國代表大會(huì)及學(xué)術(shù)會(huì)議論文摘要[C];2010年

5 江鍵;崔黎麗;宋誠榮;王小平;宋茂海;;負(fù)極性駐極體誘導(dǎo)3T3細(xì)胞表面電荷和游離鈣濃度的變化[A];第四屆中國功能材料及其應(yīng)用學(xué)術(shù)會(huì)議論文集[C];2001年

6 梁冀;于會(huì)梅;傅繼東;郭昂;楊黃恬;;內(nèi)質(zhì)網(wǎng)鈣離子釋放受體對干細(xì)胞分化的調(diào)控[A];中國病理生理學(xué)會(huì)受體、腫瘤和免疫專業(yè)委員會(huì)聯(lián)合學(xué)術(shù)會(huì)議論文匯編[C];2010年

7 羅家江;;TH17細(xì)胞的研究進(jìn)展[A];全國中西醫(yī)結(jié)合血液學(xué)學(xué)術(shù)會(huì)議論文匯編[C];2010年

8 項(xiàng)盈;金潔;沈丹;鄭強(qiáng);謝純剛;賈冰冰;黃國平;王金福;;復(fù)蘇的人骨髓間充質(zhì)干細(xì)胞的分離、培養(yǎng)及向多系細(xì)胞分化的誘導(dǎo)[A];第10屆全國實(shí)驗(yàn)血液學(xué)會(huì)議論文摘要匯編[C];2005年

9 汪洋;朱椰凡;余華軍;符竣惠;徐啟綱;曾其強(qiáng);吳建波;張啟瑜;;三種全肝臟去細(xì)胞化流程對細(xì)胞外基質(zhì)的影響及細(xì)胞組分殘留量的研究[A];2013年浙江省外科學(xué)學(xué)術(shù)年會(huì)論文匯編[C];2013年

10 常平安;陳瑞;李薇;伍一軍;;神經(jīng)病靶標(biāo)酯酶的增強(qiáng)表達(dá)抑制哺乳動(dòng)物細(xì)胞的增殖[A];中國環(huán)境誘變劑學(xué)會(huì)抗誘變劑和抗癌劑專業(yè)委員會(huì)第三次全國學(xué)術(shù)會(huì)議、中國毒理學(xué)會(huì)生化與分子毒理專業(yè)委員會(huì)第五屆學(xué)術(shù)交流會(huì)、貴州省環(huán)境誘變劑學(xué)會(huì)成立大會(huì)暨首屆學(xué)術(shù)交流會(huì)論文集[C];2004年

相關(guān)重要報(bào)紙文章 前10條

1 徐榮祥;人類生命細(xì)胞 再生物質(zhì)的發(fā)現(xiàn)與研究[N];健康報(bào);2007年

2 張佳星;干細(xì)胞分化路徑存在差異性[N];中國礦業(yè)報(bào);2008年

3 史軍;剝開黏合的細(xì)胞之書[N];健康報(bào);2012年

4 常麗君;美生物學(xué)家打造出“細(xì)胞黑客”[N];科技日報(bào);2010年

5 張佳星;分化之路 殊途同歸[N];科技日報(bào);2008年

6 記者 施嘉奇　通訊員 王姿英;探索中藥對干細(xì)胞分化的作用[N];文匯報(bào);2009年

7 記者陳超;日開發(fā)細(xì)胞間隔離培養(yǎng)技術(shù)[N];科技日報(bào);2003年

8 陳超;科學(xué)家發(fā)現(xiàn)引發(fā)細(xì)胞分化的分子通道[N];科技日報(bào);2010年

9 記者 白毅;我國科學(xué)家用iPS細(xì)胞首獲克隆豬[N];中國醫(yī)藥報(bào);2013年

10 記者 錢錚;日本用人類iPS細(xì)胞首次制成血小板[N];新華每日電訊;2009年

相關(guān)博士學(xué)位論文 前10條

1 唐紹燦;IL-27、Th1及Th17細(xì)胞在MS中的表達(dá)及其作用機(jī)制研究[D];山東大學(xué);2015年

2 常凱凱;子宮內(nèi)膜異位灶微環(huán)境IL-10~+Th17細(xì)胞的形成及作用機(jī)制[D];復(fù)旦大學(xué);2014年

3 高華嵩;細(xì)胞重編程技術(shù)和移植治療視神經(jīng)損傷的實(shí)驗(yàn)研究[D];復(fù)旦大學(xué);2014年

4 李艷明;Hsa-miR-200a調(diào)控紅細(xì)胞分化的功能及分子機(jī)制研究[D];中國科學(xué)院北京基因組研究所;2015年

5 張林;C-反應(yīng)蛋白通過對T細(xì)胞分化的直接調(diào)控參與后天免疫應(yīng)答[D];蘭州大學(xué);2015年

6 蔣云秋;樹突狀細(xì)胞Notch信號在1，，25-二羥維生素D3調(diào)節(jié)Th17分化中的作用研究[D];第三軍醫(yī)大學(xué);2015年

7 史莉瑾;急性腦出血患者外周血調(diào)節(jié)性T細(xì)胞與腦相關(guān)抗原的特征及其相關(guān)性研究[D];鄭州大學(xué);2015年

8 陳博;可注射細(xì)胞微球明膠復(fù)合物聯(lián)合血小板裂解液在牙組織工程中的應(yīng)用研究[D];第四軍醫(yī)大學(xué);2015年

9 章麗雅;血紅素加氧酶-1調(diào)抑Th17細(xì)胞在炎癥性腸病中的作用及機(jī)制研究[D];上海交通大學(xué);2013年

10 曹際森;miR-146a調(diào)控Treg細(xì)胞抑制小鼠心臟移植免疫排斥的研究[D];天津醫(yī)科大學(xué);2015年

相關(guān)碩士學(xué)位論文 前10條

1 周明;As_2O_3聯(lián)合γ分泌酶抑制劑影響肝癌HepG_2細(xì)胞耐藥性的研究[D];石河子大學(xué);2015年

2 劉冰慧;凋亡細(xì)胞對巨噬細(xì)胞IL-12家族細(xì)胞因子調(diào)控的研究[D];河北醫(yī)科大學(xué);2015年

3 韓青青;Th22細(xì)胞及其效應(yīng)因子IL-22與類風(fēng)濕關(guān)節(jié)炎及合并間質(zhì)性肺病相關(guān)性的研究[D];河北醫(yī)科大學(xué);2015年

4 張騰飛;吉西他濱與AMD3100聯(lián)合應(yīng)用于膽管癌RBE細(xì)胞株對CXCR4/CXCL12軸的作用[D];河北醫(yī)科大學(xué);2015年

5 王們X ;EAAL細(xì)胞聯(lián)合全反式維甲酸對人肺腺癌細(xì)胞株A549體內(nèi)外作用的研究[D];河北醫(yī)科大學(xué);2015年

6 李超楠;兩種典型OPFRs對PC12細(xì)胞的神經(jīng)毒性及其機(jī)制探究[D];中國人民解放軍軍事醫(yī)學(xué)科學(xué)院;2015年

7 楊明;促腎上腺皮質(zhì)激素釋放因子1型受體經(jīng)cAMP/PKA信號通路對U87MG細(xì)胞凋亡機(jī)制的研究[D];河北醫(yī)科大學(xué);2015年

8 周新宇;miR143、miR145對C2C12細(xì)胞分化的影響作用研究[D];四川農(nóng)業(yè)大學(xué);2015年

9 李姝;淫羊藿苷對胃癌SGC-7901細(xì)胞內(nèi)CaSR及Survivin、Runx3基因表達(dá)的影響[D];甘肅中醫(yī)藥大學(xué);2016年

10 金瑛;體外誘導(dǎo)人羊膜間充質(zhì)干細(xì)胞向韌帶細(xì)胞分化的實(shí)驗(yàn)研究[D];遵義醫(yī)學(xué)院;2016年

本文編號：2006689