【摘要】：目的:1研究MiCroRNA-23a在胰腺癌組織中的表達(dá)情況及其與臨床病理資料的關(guān)系。2研究MiCroRNA-23a在不同胰腺癌細(xì)胞株(Aspc-1,Bxpc-3,Cfpac-1,Panc-1)的表達(dá)規(guī)律。3研究MiCroRNA-23a體內(nèi)體外促進(jìn)胰腺癌細(xì)胞侵襲轉(zhuǎn)移。4研究MiCroRNA-23a通過靶向抑制上皮剪接調(diào)節(jié)蛋白1(epithelial splicing regulator protein 1,ESRP1)改變CD44亞型表達(dá),促進(jìn)胰腺癌細(xì)胞發(fā)生上皮間質(zhì)轉(zhuǎn)化(epithelial mesenchymal transition,EMT),促進(jìn)胰腺癌細(xì)胞侵襲轉(zhuǎn)移。方法:1.收集西南醫(yī)院肝膽外科2013年1月~2013年12月手術(shù)切除的胰腺癌標(biāo)本及患者臨床病理資料共計47例,記錄患者FOS及OS。采用RT-PCR方法檢測MiCro RNA-23a在胰腺癌原發(fā)灶,轉(zhuǎn)移淋巴結(jié)組織以及癌旁正常胰腺組織中的表達(dá)情況,比較MiCroRNA-23a在上述三種組織中的表達(dá)差異。計算癌組織中MiCro RNA-23a的相對平均表達(dá)量,并根據(jù)該值將所有標(biāo)本分為MiCroRNA-23a高表達(dá)組和低表達(dá)組,分析MiCroRNA-23a表達(dá)與臨床病理資料的關(guān)系。采用Kaplan-Meier軟件進(jìn)行生存分析,研究不同表達(dá)水平的MiCro RNA-23a對胰腺癌患者預(yù)后的影響。2.qRT-PCR和Western blot檢測EMT標(biāo)志物E-鈣黏蛋白(E-cad),N-鈣黏蛋白(N-cad),波形蛋白(VIM)的表達(dá),觀察細(xì)胞形態(tài),TGF-β1誘導(dǎo)EMT處理,區(qū)分胰腺癌細(xì)胞系A(chǔ)spc-1,Bxpc-3,Cfpac-1,Panc-1的上皮、間質(zhì)表型。qRT-PCR檢測正常胰腺導(dǎo)管上皮細(xì)胞(PDC)和胰腺癌細(xì)胞(Aspc-1,Aspc-1+TGF-β1,Bxpc-3,Bxpc-3+TGF-β1,Cfpac-1,Panc-1)mi RNA-23a的表達(dá),觀察其表達(dá)與胰腺癌細(xì)胞EMT表型的關(guān)系。干擾mi R-23a,觀察對TGF-β1誘導(dǎo)EMT的影響。3.miR-23a mimic和mi R-23a inhibitor分別轉(zhuǎn)染Aspc-1和Panc-1,觀察其侵襲遷移能力的變化;構(gòu)建mi R-23a sponges慢病毒表達(dá)載體,轉(zhuǎn)染Panc-1細(xì)胞,建立穩(wěn)定細(xì)胞株,裸鼠體內(nèi)實驗觀察mi R-23a促進(jìn)胰腺癌轉(zhuǎn)移。4.基因芯片分析和生物信息學(xué)網(wǎng)站(TargetScan.com)搜索結(jié)果交叉比較,雙熒光素酶報告質(zhì)粒實驗驗證ESRP1是mi R-23a的直接靶基因。5.研究干擾miR-23a對ESRP1表達(dá)的影響,qRT-PCR檢測胰腺癌組織ESRP1的表達(dá),與miR-23a的表達(dá)進(jìn)行相關(guān)性分析;干擾或過表達(dá)ESRP1,觀察對胰腺癌細(xì)胞侵襲轉(zhuǎn)移能力的影響;ESRP1回復(fù)實驗,觀察對mi R-23a影響胰腺癌細(xì)胞EMT的逆轉(zhuǎn)作用。6.Western blot、qRT-PCR分別檢測mi R-23a對ESRP1及其下游CD44s/CD44v、FGFR2 IIIb/IIIc剪接亞型表達(dá)的影響。ESRP1回復(fù)實驗觀察干擾mi R-23a表達(dá)對下游剪接分子表達(dá)的影響。結(jié)果:1.胰腺癌轉(zhuǎn)移淋巴結(jié)組織中mi R-23a的表達(dá)顯著高于胰腺癌原發(fā)灶和癌旁正常組織,胰腺癌MiCroRNA-23a表達(dá)與腫瘤組織分化程度、腫瘤浸潤深度(T分期)以及胰腺癌淋巴結(jié)轉(zhuǎn)移(N分期)具有顯著相關(guān)性,而其表達(dá)與年齡、性別,腫瘤發(fā)生部位及遠(yuǎn)處轉(zhuǎn)移(M分期)等無相關(guān)性。生存分析發(fā)現(xiàn),MiCroRNA-23a表達(dá)與胰腺癌腫瘤患者預(yù)后具有相關(guān)性,高表達(dá)組預(yù)后差,生存期均低于低表達(dá)組,兩者相比較差異具有統(tǒng)計學(xué)意義。2.1 Aspc-1、Bxpc-3細(xì)胞呈上皮表型,Cfpac-1、Panc-1為間質(zhì)表型,TGF-β1誘導(dǎo)Aspc-1、Bxpc-3后,發(fā)生EMT。miR-23a在間質(zhì)表型的胰腺癌細(xì)胞中表達(dá)明顯增高。結(jié)合mi R-23a在胰腺癌轉(zhuǎn)移淋巴結(jié)組織中表達(dá)增高,推測miR-23a可能促進(jìn)胰腺癌細(xì)胞上皮間質(zhì)轉(zhuǎn)化及侵襲轉(zhuǎn)移。干擾mi R-23a,抑制了TGF-β1誘導(dǎo)上皮表型胰腺癌細(xì)胞EMT的發(fā)生。3.體外實驗證明,mi R-23a mimic轉(zhuǎn)染Aspc-1導(dǎo)致其侵襲遷移能力增強,mi R-23a inhibitor轉(zhuǎn)染Panc-1導(dǎo)致其侵襲遷移能力減弱;體內(nèi)實驗證明,mi R-23a sponges慢病毒表達(dá)載體轉(zhuǎn)染Panc-1細(xì)胞,可以抑制miR-23a的功能,從而抑制胰腺癌細(xì)胞生長及轉(zhuǎn)移。4.基因芯片分析及生物信息學(xué)檢索,證實ESRP1是miR-23a的直接的下游靶基因,熒光素酶報告質(zhì)粒實驗證實ESRP1是mi R-23a的直接靶基因。5.ESRP1維持胰腺癌細(xì)胞的上皮表型,干擾mi R-23a,ESRP1的表達(dá)發(fā)生變化;胰腺癌組織中,ESRP1的表達(dá)與miR-23a的表達(dá)呈顯著負(fù)相關(guān)。ESRP1si RNA轉(zhuǎn)染Aspc-1后導(dǎo)致其侵襲遷移能力增強;ESRP1過表達(dá)質(zhì)粒轉(zhuǎn)染Panc-1后導(dǎo)致其侵襲遷移能力減弱。ESRP1回復(fù)實驗,可以部分逆轉(zhuǎn)干擾mi R-23a表達(dá)后對胰腺癌細(xì)胞EMT的影響。6.qRT-PCR、WB檢測證實mi R-23a靶向抑制ESRP1的表達(dá),從而導(dǎo)致下游剪接分子CD44s/CD44v、FGFR2 IIIb/IIIc的表達(dá)變化,ESRP1回復(fù)實驗可以部分逆轉(zhuǎn)干擾mi R-23a表達(dá)對下游剪接分子表達(dá)的影響。結(jié)論:1.MiCroRNA-23a在胰腺癌淋巴結(jié)轉(zhuǎn)移灶中的表達(dá)明顯高于胰腺癌原發(fā)灶及癌旁正常胰腺組織,MiCroRNA-23a表達(dá)與腫瘤分化程度、腫瘤浸潤深度以及胰腺癌淋巴結(jié)轉(zhuǎn)移呈顯著正相關(guān),MiCroRNA-23a表達(dá)與胰腺癌預(yù)后具有顯著相關(guān)性。2.上皮表型胰腺癌細(xì)胞低表達(dá)MiCro RNA-23a,間皮表型胰腺癌細(xì)胞高表達(dá)MiCroRNA-23a,當(dāng)上皮表型的胰腺癌細(xì)胞發(fā)生EMT時,MiCroRNA-23a的表達(dá)顯著增高,因此MiCroRNA-23a可能促進(jìn)了胰腺癌細(xì)胞EMT。3.過表達(dá)MiCroRNA-23a能夠促進(jìn)胰腺癌細(xì)胞由上皮表型向間質(zhì)表型轉(zhuǎn)化;抑制MiCroRNA-23a表達(dá)能夠促進(jìn)胰腺癌細(xì)胞由間質(zhì)表型向上皮表型轉(zhuǎn)化。4.MiCroRNA-23a能夠增強胰腺癌細(xì)胞體外培養(yǎng)細(xì)胞以及裸鼠體內(nèi)的侵襲轉(zhuǎn)移能力。5.MiCroRNA-23a通過靶向抑制ESRP1的表達(dá)對胰腺癌細(xì)胞上皮間質(zhì)轉(zhuǎn)化發(fā)揮調(diào)控作用,從而促進(jìn)胰腺癌細(xì)胞侵襲轉(zhuǎn)移。6.ESRP1通過調(diào)控CD44s/CD44v選擇性剪接以及FGFR2IIIb/IIIc分子的表達(dá)變化影響胰腺癌細(xì)胞上皮間質(zhì)轉(zhuǎn)化。
[Abstract]:Objective: 1 to study the expression of MiCroRNA-23a in pancreatic carcinoma and its relationship with clinicopathological data.2 study on the expression of MiCroRNA-23a in different pancreatic cancer cell lines (Aspc-1, Bxpc-3, Cfpac-1, Panc-1).3 research MiCroRNA-23a in vivo and in vitro promoting the invasion and metastasis of pancreatic cancer cells in vitro,.4 MiCroRNA-23a through targeted inhibition of epithelium Splicing regulation protein 1 (epithelial splicing regulator protein 1, ESRP1) changes the expression of CD44 subtype and promotes epithelial mesenchymal transformation of pancreatic cancer cells (epithelial mesenchymal transition, EMT), and promotes invasion and metastasis of pancreatic cancer cells. Methods: 1. collection of pancreatic cancer markers in Department of hepatobiliary surgery, Southwest Hospital, January 2013 ~2013 year December. This and the patient's clinicopathological data were 47 cases. The FOS and OS. were recorded by RT-PCR method to detect the expression of MiCro RNA-23a in the primary pancreatic cancer, the metastasis lymph node tissue and the normal pancreatic tissue adjacent to the carcinoma. The difference of the expression of MiCroRNA-23a in the above three tissues was compared. The relative average of MiCro RNA-23a in the cancer tissue was calculated. According to this value, all the specimens were divided into MiCroRNA-23a high expression group and low expression group. The relationship between MiCroRNA-23a expression and clinicopathological data was analyzed. Kaplan-Meier software was used to carry out survival analysis, and the effects of MiCro RNA-23a on the prognosis of pancreatic cancer patients with different expression levels were detected by.2.qRT-PCR and Western blot to detect EMT marker E-. The expression of calcium mucin (E-cad), N- calcium mucin (N-cad) and vimentin (VIM), observed cell morphology, TGF- beta 1 induced EMT treatment, differentiating the epithelium of pancreatic cancer cell lines Aspc-1, Bxpc-3, Cfpac-1, Panc-1,.QRT-PCR detection of normal pancreatic duct epithelial cells (PDC) and pancreatic cancer cells (PDC) and pancreatic cancer cells. PAC-1, Panc-1) mi RNA-23a expression and the relationship between the expression of EMT and the EMT phenotype of pancreatic cancer cells. Interfering mi R-23a, and observing the effect of TGF- beta 1 on EMT induced by.3.miR-23a mimic and MI. To establish a stable cell line, the experimental observation of MI R-23a in nude mice to promote pancreatic cancer metastasis.4. gene chip analysis and bioinformatics website (TargetScan.com) search results cross comparison, double luciferase reporter plasmid experiment verifying that ESRP1 is the direct target gene.5. of MI R-23a to study the effect of dry disturbance miR-23a on ESRP1 expression, qRT-PCR detection of the pancreas The expression of ESRP1 in the carcinoma tissue was correlated with the expression of miR-23a, and the effect of ESRP1 on the invasion and metastasis of pancreatic cancer cells was observed, and ESRP1 recovery experiment was used to observe the reverse effect of MI R-23a on the EMT in pancreatic cancer cells.6.Western blot, qRT-PCR division and MI R-23a. The effect of the expression of MI R-23a on the expression of the downstream splicing molecules was disturbed by the expression of b/IIIc splice subtype. Results: 1. the expression of MI R-23a in the metastatic lymph nodes of pancreatic cancer was significantly higher than that of the primary pancreatic cancer and the normal tissue adjacent to the carcinoma. The MiCroRNA-23a table of the pancreatic cancer was associated with the degree of differentiation of the tumor tissue and the depth of the tumor (the depth of the tumor). There was a significant correlation between T staging and lymph node metastasis (N staging) of pancreatic cancer. The expression was not related to age, sex, tumor site and distant metastasis (M staging). Survival analysis showed that the expression of MiCroRNA-23a was related to the prognosis of pancreatic cancer patients. The prognosis of the high expression group was poor and the survival time was lower than that of the low expression group. The difference was statistically significant.2.1 Aspc-1, Bxpc-3 cells were epithelial phenotype, Cfpac-1, Panc-1 were interstitial phenotypes, TGF- beta 1 induced Aspc-1, Bxpc-3, and EMT.miR-23a expressed significantly in the pancreatic cancer cells with interstitial phenotypes. Mi R-23a in pancreatic cancer metastatic lymph node tissues increased, presumably that miR-23a may promote pancreas Epithelial mesenchymal transformation and invasion and metastasis of adenocarcinoma cells interfere with MI R-23a and inhibit the occurrence of EMT in epithelial pancreatic cancer cells induced by TGF- beta 1 in vitro..3. in vitro experiments show that MI R-23a mimic transfected Aspc-1 leads to the enhancement of its invasion and migration ability, MI R-23a inhibitor, which leads to the weakening of its invasion and migration ability. The transfection of NGEs Lentivirus Expression Vector to Panc-1 cells inhibits the function of miR-23a and inhibits the growth and metastasis of pancreatic cancer cells and.4. gene chip analysis and bioinformatics retrieval. It is proved that ESRP1 is a direct downstream target gene of miR-23a, and the luciferase reporter plasmid experiment confirms that ESRP1 is the direct target gene of MI R-23a to maintain the pancreas. The epithelial phenotype of adenocarcinoma cells interfered with MI R-23a and the expression of ESRP1. In pancreatic cancer tissue, the expression of ESRP1 and miR-23a expressed a significant negative correlation with.ESRP1si RNA transfection to Aspc-1, resulting in enhanced invasion and migration ability; ESRP1 overexpression plasmid transfected to Panc-1 led to its invasion and migration ability to weaken.ESRP1 response experiment. The effect of MI R-23a expression on the EMT of pancreatic cancer cells.6.qRT-PCR. WB detection confirmed that MI R-23a target inhibited the expression of ESRP1, which led to the expression of CD44s/CD44v and FGFR2 IIIb/IIIc in the downstream splicing molecules, and the ESRP1 response experiment could partly reverse the influence of the expression of the downstream splice molecules. The expression of roRNA-23a in the lymph node metastasis of pancreatic cancer was significantly higher than that of the primary pancreatic cancer and the normal pancreatic tissue near the carcinoma. The expression of MiCroRNA-23a was significantly correlated with the degree of tumor differentiation, the depth of tumor invasion and the lymph node metastasis of pancreatic cancer. The expression of MiCroRNA-23a was significantly correlated with the.2. epithelial phenotype of pancreatic cancer. The cells expressed low expression of MiCro RNA-23a, and the mesothelial phenotype of pancreatic cancer cells expressed MiCroRNA-23a. When the epithelial phenotype of pancreatic cancer cells was EMT, the expression of MiCroRNA-23a was significantly increased. Therefore, MiCroRNA-23a may promote the EMT.3. overexpression of pancreatic cancer cells to promote the transformation of pancreatic cancer cells from the epithelial phenotype to the interstitial phenotype. Inhibition of MiCroRNA-23a expression can promote the transformation of pancreatic cancer cells from the interstitial phenotype to the epithelial phenotype..4.MiCroRNA-23a can enhance the invasion and metastasis ability of pancreatic cancer cells in vitro and in nude mice..5.MiCroRNA-23a can play a regulatory role in the transformation of pancreatic carcinoma cells through the target inhibition of ESRP1 expression. The invasion and metastasis of pancreatic cancer cells.6.ESRP1 affects the epithelial mesenchymal transition of pancreatic cancer cells by regulating the selective splicing of CD44s/CD44v and the expression of FGFR2IIIb/IIIc molecules.
【學(xué)位授予單位】：第三軍醫(yī)大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：R735.9

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