当前位置:主页 > 科技论文 > 基因论文 >

食管鳞癌组织中自噬相关基因9B mRNA及蛋白的表达变化

发布时间:2018-04-29 13:10

  本文选题:食管肿瘤 + 食管癌 ; 参考:《山东医药》2017年15期


【摘要】:目的观察食管鳞癌(ESCC)组织中自噬相关基因(ATG9B)9B mRNA及蛋白的表达变化,并探讨其意义。方法食管癌切除术中切取的新鲜ESCC组织及癌旁正常黏膜组织各70例份,采用qRT-PCR法检测ATG9B mRNA。收集198例份食管癌根治切除术留取的ESCC组织及癌旁正常黏膜组织标本构建组织芯片,采用免疫组化法检测ATG9B蛋白,分析ATG9B蛋白表达与ESCC临床病理参数的关系。结果 ESCC组织、正常食管黏膜组织中ATG9B mRNA相对表达量分别为0.303±0.197、1.186±0.642,ESCC组织中ATG9B mRNA相对表达量低于正常食管黏膜组织(P0.05)。ESCC组织中ATG9B蛋白阳性表达率低于正常食管黏膜组织(分别为32.6%、60.5%,P0.05)。ATG9B蛋白在高、中、低分化ESCC组织中阳性表达率依次降低,在Ⅰ~Ⅱ期肿瘤组织中的阳性表达率高于Ⅲ~Ⅳ期组织(P均0.05)。结论 ESCC组织中ATG9B mRNA及蛋白表达均低于正常食管黏膜组织;ATG9B表达下调可能与ESCC的发生发展有关。
[Abstract]:Objective to investigate the expression of ATG9Bn9B mRNA and protein in esophageal squamous cell carcinoma (ESCC) and its significance. Methods A total of 70 fresh ESCC tissues and 70 adjacent normal mucosa tissues were collected during resection of esophageal carcinoma. ATG9B mRNA was detected by qRT-PCR method. The tissue microarray was constructed from 198 specimens of ESCC tissue and normal mucosa adjacent to esophageal carcinoma after radical resection of esophageal carcinoma. The expression of ATG9B protein was detected by immunohistochemical method. The relationship between the expression of ATG9B protein and the clinicopathological parameters of ESCC was analyzed. Results ESCC tissue, The relative expression of ATG9B mRNA in normal esophageal mucosa was 0.303 卤0.197 1.186 卤0.642ESCC was lower than that in normal esophageal mucosal tissue P0.05. ATG9B protein positive rate was lower than that in normal esophageal mucosa tissue (32.60.75%, P 0.05%. ATG9B protein was higher than that in normal esophageal mucosal tissue (32.60.75%, P 0.05%). ATG9B protein in normal esophageal mucosa tissue was higher than that in normal esophageal mucosal tissue (32.60.75%, P 0.05 .ATG9B protein, respectively). The positive expression rate of ESCC in stage 鈪,

本文编号:1820071

资料下载
论文发表

本文链接:https://www.wllwen.com/kejilunwen/jiyingongcheng/1820071.html


Copyright(c)文论论文网All Rights Reserved | 网站地图 |

版权申明:资料由用户4d190***提供,本站仅收录摘要或目录,作者需要删除请E-mail邮箱bigeng88@qq.com