非編碼RNAs miR-141/miR-22和PVT1調(diào)控胃癌生長和轉(zhuǎn)移的作用與機(jī)制研究
發(fā)布時間：2021-06-22 02:59
研究背景與意義:胃癌（gastric cancer）是世界范圍內(nèi)第五大流行的惡性腫瘤,同時其引起的相關(guān)死亡在癌癥領(lǐng)域內(nèi)位列第三。據(jù)2015年發(fā)表的《Global cancer statistics,2012》的最新統(tǒng)計(jì)數(shù)據(jù)顯示:在2012年全球范圍內(nèi)預(yù)估胃癌新發(fā)患者有951600例,胃癌患者死亡病例為723100例。盡管在胃癌的診斷治療領(lǐng)域取得了不斷的進(jìn)展,但我國胃癌患者的5年生存率仍舊較低,且惡性胃癌的中位生存期仍然沒有顯著的提高。因此,深入研究胃癌發(fā)生進(jìn)程中的分子機(jī)制,為胃癌患者提供新的診斷治療方式和策略具有重要的意義。芯片和高通量測序技術(shù)對基因組和轉(zhuǎn)錄組學(xué)的研究表明僅少于2%的基因組用來編碼蛋白,而大于75%的基因組被激活轉(zhuǎn)錄為非編碼RNAs。新近研究表明,腫瘤基因組中的多個突變位點(diǎn)位于非編碼蛋白的區(qū)域,而這些區(qū)域通常會轉(zhuǎn)錄為微小RNAs（mi RNAs）和長鏈非編碼RNAs（long non-coding RNAs,lncRNAs）。二代測序結(jié)果表明,多個miRNAs和lncRNAs的表達(dá)異常與多種腫瘤的發(fā)生與進(jìn)程相關(guān),這些異常表達(dá)的mi RNAs和lncRNAs在基因表達(dá)調(diào)控...
【文章來源】：中國人民解放軍陸軍軍醫(yī)大學(xué)重慶市
【文章頁數(shù)】：147 頁
【學(xué)位級別】：博士
【部分圖文】：
miR-141在胃癌組織中表達(dá)下調(diào)，其表達(dá)與胃癌的轉(zhuǎn)移能力成負(fù)相關(guān)Figure1.MiR-141isdownregulatedinprimarytumortissuesofGCandcorrelatesinverselywithmetastaticcapacityinGCtissue.（A）Differentialexpressionof16miRNAsbetweenpairedGCandnormalmucosa（NM）
37圖 2. miR-141 的過表達(dá)抑制胃癌細(xì)胞系的增殖，侵襲和遷移Figure 2. The effect of ectopic expression of miR-141 levels on cell proliferation, migration andinvasion of HGC-27 in vitro.（A） MiR-141 effectively increased miR-141 expression level, as determined using real time PCRin HGC-27 cell line, which was normalized against U6 RNA. Data are presented as mean±S.D. （n= 3）.（B）Overexpression of miR-141 by miR-141 mimics affected the cell proliferation of HGC-27 cells asdetermined using CCK8 assay. Data are presented as mean±S.D. （n= 6）. （C, D） Overexpression ofmiR-141 by miR-141 mimics affects the migration capacity of HGC-27 cells as determined using theWound healing assay. Representative images were captured at 0 h and 48 h after transfection. Therelative wound breadth remain （100%） represents the migration capacity of gastric cancer cells, andthe breadth at 0 h was set as 100%. All of the experiments were performed three times. Data are
39圖 3. 抑制 miR-141 的表達(dá)，促進(jìn)胃癌細(xì)胞系 AGS 細(xì)胞的增殖，遷移和侵襲Figure 3. The effect of inhibition of miR-141 levels on cell proliferation,migration and invasion of AGS in vitro.（A）MiR-141 inhibitors effectively decreased miR-141 expression level, as determined using realtime PCR in AGS cell line, which was normalized against U6 RNA. Data are presented as mean±S.D.（n= 3）. （B） Inhibition of miR-141 by miR-141inhibitors affected the cell proliferation of AGS cellsas determined using CCK8 assay. Data are presented as mean±S.D. （n= 6）. （C, D） Inhibition ofmiR-141 by miR-141 inhibitors affects the migration capacity of AGS cells as determined using theWound healing assay. Representative images were captured at 0 h and 48 h after transfection. Therelative wound breadth remain （100%） represents the migration capacity of gastric cancer cells, andthe breadth at 0 h was set as 100%. All of the experiments were performed three times. Data are
本文編號：3241974
【文章來源】：中國人民解放軍陸軍軍醫(yī)大學(xué)重慶市
【文章頁數(shù)】：147 頁
【學(xué)位級別】：博士
【部分圖文】：
miR-141在胃癌組織中表達(dá)下調(diào)，其表達(dá)與胃癌的轉(zhuǎn)移能力成負(fù)相關(guān)Figure1.MiR-141isdownregulatedinprimarytumortissuesofGCandcorrelatesinverselywithmetastaticcapacityinGCtissue.（A）Differentialexpressionof16miRNAsbetweenpairedGCandnormalmucosa（NM）
37圖 2. miR-141 的過表達(dá)抑制胃癌細(xì)胞系的增殖，侵襲和遷移Figure 2. The effect of ectopic expression of miR-141 levels on cell proliferation, migration andinvasion of HGC-27 in vitro.（A） MiR-141 effectively increased miR-141 expression level, as determined using real time PCRin HGC-27 cell line, which was normalized against U6 RNA. Data are presented as mean±S.D. （n= 3）.（B）Overexpression of miR-141 by miR-141 mimics affected the cell proliferation of HGC-27 cells asdetermined using CCK8 assay. Data are presented as mean±S.D. （n= 6）. （C, D） Overexpression ofmiR-141 by miR-141 mimics affects the migration capacity of HGC-27 cells as determined using theWound healing assay. Representative images were captured at 0 h and 48 h after transfection. Therelative wound breadth remain （100%） represents the migration capacity of gastric cancer cells, andthe breadth at 0 h was set as 100%. All of the experiments were performed three times. Data are
39圖 3. 抑制 miR-141 的表達(dá)，促進(jìn)胃癌細(xì)胞系 AGS 細(xì)胞的增殖，遷移和侵襲Figure 3. The effect of inhibition of miR-141 levels on cell proliferation,migration and invasion of AGS in vitro.（A）MiR-141 inhibitors effectively decreased miR-141 expression level, as determined using realtime PCR in AGS cell line, which was normalized against U6 RNA. Data are presented as mean±S.D.（n= 3）. （B） Inhibition of miR-141 by miR-141inhibitors affected the cell proliferation of AGS cellsas determined using CCK8 assay. Data are presented as mean±S.D. （n= 6）. （C, D） Inhibition ofmiR-141 by miR-141 inhibitors affects the migration capacity of AGS cells as determined using theWound healing assay. Representative images were captured at 0 h and 48 h after transfection. Therelative wound breadth remain （100%） represents the migration capacity of gastric cancer cells, andthe breadth at 0 h was set as 100%. All of the experiments were performed three times. Data are
本文編號：3241974
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