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胃癌是我国常见的恶性肿瘤之一,在我国其发病率仅次于肺癌.每年约有17万人死于胃癌.肿瘤转移是多步骤多分子参与的过程.上皮细胞向间充质细胞转化(EMT)是激发肿瘤细胞转移的关键.确认参与EMT转化的关键分子,理解EMT形成机制是积极预防肿瘤转移,提高晚期恶性肿瘤治疗方法的重要研究方向.近年来,随着基因测序技术的不断进步,人类基因中发现越来越多非编码RNA与恶性肿瘤的形成、侵袭及转移密切相关,非编码RNA中的长链非编码RNA(lncRNA)得到了广泛关注.LncRNAs在胃癌进展及转移中同样发挥着有力的调控作用.本文专注于分析与胃癌EMT相关的lncRNAs,这些lncRNA通过影响蛋白降解,转录控制以及调控miRNA以促进EMT发生,从而介导肿瘤的转移.基于目前研究基础,真正阐明lncRNA与胃癌转移的机制还有很多未知,需要进一步去发现. 相似文献
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Twist在胃癌黏膜组织的表达及在上皮间质转化中的作用 总被引:1,自引:0,他引:1
目的:观察上皮间质转化因子Twist在胃癌中的表达情况以及与胃癌恶性生物学行为的相关性。方法:采用免疫组化SP法检测59例胃癌组织中Twist,上皮源性标记物E-cadherin,间叶源性标记物Vimentin的表达,并分析与各临床病理因素之间的关系。结果:59例胃癌组织中Twist阳性表达率为74.6%(44/59),29例观察到E-cadherin表达的降低,同时7例观察到Vimentin表达上调。Twist的表达与淋巴结转移密切相关(P<0.05);而且Twist表达与E-cadherin表达降低(P<0.05)和Vimentin的表达上调(P<0.05)之间都存在相关性。结论:Twist可能通过调控上皮间质转化从而在胃癌的侵袭转移过程中发挥作用。 相似文献
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上皮间质转化(EMT)在结肠癌发生发展、侵袭转移中发挥重要作用.转化生长因子-β、Wnt/β-catein、Notch、核转录因子-κB、磷脂酰肌醇-3激酶/蛋白激酶B信号通路对结肠癌EMT过程起重要的诱导调控作用.进一步阐明EMT信号通路,可为结肠癌靶向治疗带来更多的机会. 相似文献
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目的:探讨CTEN在乳腺癌细胞上皮间质转化中的作用及其分子机制。方法:采用定量PCR及Western blotting检测人乳腺癌MCF-7和MDA-MB-231细胞中CTEN的表达水平;然后用Lipofectamine 2000将CTEN高表达质粒pcmv-CTEN转染至乳腺癌MCF-7细胞,为高表达组,将对照质粒pcmv转染至MCF-7细胞,为对照组,用定量PCR检测两组细胞中CTEN、Snail和EMT标记分子mRNA水平的变化,用Western blotting检测CTEN、Snail和EMT标记分子蛋白水平的变化;应用Lipofectamine 2000将CTEN干扰质粒siCTEN转染至MDA-MB-231细胞,为干扰组,将对照质粒siNC转染至MDA-MB-231细胞,为对照组,分别用定量PCR和Western blotting检测两组细胞中CTEN、Snail和EMT标记分子mRNA及蛋白水平的变化;应用Lipofectamine 2000将Snail干扰质粒siSnail转染至MCF-7细胞,为干扰组,将对照质粒siNC转染至MCF-7细胞,为对照组,分别用定量PCR和Western blotting检测两组细胞中Snail mRNA及蛋白水平的表达情况,然后再将CTEN高表达质粒pcmv-CTEN转染入两组细胞,定量PCR检测CTEN和EMT标记分子mRNA水平的变化,Western blotting检测CTEN和EMT标记分子蛋白水平的变化。结果:CTEN在MDA-MB-231中的表达量高于MCF-7细胞;与对照组相比,高表达CTEN组的MCF-7细胞形态呈纺锥形,Snail表达升高,上皮标记分子E-cadherin表达下降,间质标记分子N-cadherin及Vimentin表达升高,促进EMT的发生;与对照组相比,敲低CTEN组的MDA-MB-231细胞形态呈鹅卵石形,Snail表达下降,上皮标记分子E-cadherin表达上升,间质标记分子N-cadherin及Vimentin表达下降,促进MET的发生;在MCF-7细胞中干扰Snail后再过表达CTEN,其促进EMT的作用明显减弱。结论:CTEN能够诱导乳腺癌细胞发生上皮间质转化,且其可能通过转录因子Snail发挥作用。 相似文献
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《European journal of cancer (Oxford, England : 1990)》2014,50(1):204-215
Gastric cancer is the second most fatal common form of cancer. The crosstalk among signalling pathways that results in the acceleration of epithelial to mesenchymal transition (EMT) plays a pivotal role in the molecular mechanism of gastric carcinogenesis. To understand the role of caveolin-1 (Cav-1), the expression pattern was studied in human gastric adenocarcinoma tissues and also in AGS and KATO III cell lines. Here, we show that during hypoxic condition, the increase in the levels of hypoxia-inducible factor-1α (HIF-1α) results in a significant decrease in the expression of caveolin-1 which is regulated by heat shock protein 90 (HSP90). The reduced levels of Cav-1 correlated with the increased epidermal growth factor receptor (EGFR) activation resulting in the significant activation of its downstream target STAT3. Accumulation of pSTAT3 in the nucleus results in the decreased expression of E-cadherin and increased expression of mesenchymal markers (Slug, α-SMA, N-cadherin and vimentin). Crosstalk of EGFR and transforming growth factor β (TGF-β) signalling with Wnt signalling enhances cell proliferation, cell survival and upregulates EMT. There was no significant alteration in the expression of epithelial and mesenchymal molecules in both the cell lines studied. Thus, we provide evidence that Cav-1 was modulated by HSP90 and functions as a crucial regulator of EMT in gastric cancer. 相似文献
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目的 探讨雷公藤内酯醇(TPL)对人胃癌细胞SGC-7901增殖、凋亡及上皮间质转化(EMT)的影响。方法 常规培养SGC-7901细胞达对数生长后,采用终浓度为12.5、25、50、100 nmol/L TPL处理SGC-7901细胞,应用四甲基偶氮唑盐比色法测定对照组及不同浓度TPL处理24、48、72和96 h的细胞增殖情况,采用流式细胞术检测不同浓度TPL处理48 h的凋亡率和细胞周期分布情况,实时荧光定量聚合酶链反应检测不同浓度TPL处理48 h的促EMT转录因子Snail1、Twist的表达情况,Western blotting检测各组处理48 h后的EMT相关标记分子(E-cadherin、N-cadherin及Vimentin)水平。结果TPL在12.5~100 nmol/L的范围内对SGC-7901细胞有增殖抑制作用,且增殖抑制率呈剂量和时间依赖性,且除24 h 12 5 nmol/L外,其余浓度及作用时间的增殖抑制率均高于对照组(P<0.05);与对照组相比,TPL处理48 h后的早晚期凋亡率升高、G0/G1期细胞比例及E-cadherin水平均升高,S期细胞比例、N-cadherin和Vimentin蛋白水平及Snail1和Twist mRNA水平均降低,差异均有统计学意义(P<0.05),且呈浓度依赖性。结论TPL对胃癌细胞SGC-7901有毒性作用,不仅抑制其增殖且诱导凋亡及细胞周期G0/G1期阻滞,同时可抑制其EMT过程。 相似文献
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Wei-Wei Li Hao Yuan Shuai Kong Shu-Bo Tian 《World journal of gastrointestinal oncology》2022,14(11):2183-2194
BACKGROUNDGastric cancer (GC) is considered a major global health problem. The role of TRIM55, a member of the three-domain protein family, in GC is unknown. AIMTo determine the expression of TRIM55 in GC tissues and its relationship with clinicopathological characteristics, and to investigate the effects of TRIM55 on the malignant biological behavior of GC cells. METHODSDifferential expression of TRIM55 in GC and para-cancer tissues was detected by immunohistochemistry, and the relationship between TRIM55 level and clinicopathological characteristics and prognosis was analyzed. Gain-of-function, loss-of-function, cell counting kit-8 assay, colony formation, transwell assay, wound healing assay, and western blot analysis were used to assess the potential role of TRIM55 in the development of GC. RESULTS TRIM55 expression was significantly increased in GC tissues compared with adjacent normal tissues. High expression of TRIM55 was associated with advanced pathological stage and poor prognosis. Overexpression of TRIM55 promoted invasion and metastasis of GC cells in vitro by regulating epithelial-mesenchymal transition (EMT), whereas knockdown of TRIM55 had the opposite effect. Our data showed that TRIM55 is highly expressed in GC tissues, and is associated with poor prognosis. TRIM55 plays the role of an oncogene in GC, and it promotes metastasis of GC through the regulation of EMT.CONCLUSION TRIM55 may be a possible target for the diagnosis and prognosis of GC patients. 相似文献
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目前越来越多的研究显示上皮间质转化(EMT)参与了肿瘤干细胞的形成以及肿瘤细胞的浸润、迁移和转移,不仅增强了癌细胞的侵袭和转移能力,还可使细胞获得自我更新等干细胞特性,促进肿瘤干细胞的产生.因此,研究EMT与常见干细胞之间的关系对于寻找控制肿瘤侵袭和转移的有效途径有非常重要的意义,亦可为肿瘤的治疗提供新的靶点. 相似文献
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上皮-间质转化(EMT)是上皮细胞向间质细胞转化的现象。近年来发现EMT可以通过多种机制影响胃癌的发生发展,促进肿瘤细胞迁移和侵袭。EMT的发生涉及多个信号通路,与微小RNA、幽门螺杆菌、转录因子等有关,其有望成为治疗侵袭性胃癌的新靶点。 相似文献
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目的:探讨lncRNA-ATB在肝癌(hepatocellular carcinoma,HCC)中的表达及意义.方法:收集2009年4月至2011年10月期间手术切除的肝癌组织以及对应的癌旁组织标本,采用real-time PCR技术分别检测lncRNA-ATB在肝癌组织与癌旁组织中的表达情况,并分析其与临床病理参数以及预后的关系.结果:lncRNA-ATB在肝癌组织中的表达水平显著高于癌旁组织,差异具有统计学意义(P<0.05);lncRNA-ATB在肝癌中的表达与淋巴结转移有关(P<0.05);lncRNA-ATB高表达组患者的预后比低表达组差.结论:lncRNA-ATB在肝癌中显著性高表达且促进肝癌的发生发展. 相似文献