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作 者:程创[1,2] 陈元武 熊伟 侯良绢[1] 夏菁 邓雪松[1,2] Cheng Chuang;Chen Yuanwu;Xiong Wei;Hou Liangjuan;Xia Jing;Deng Xuesong(Department of Human Anatomy,Chongqing Three Gorges Medical College,Chongqing 404120;Chongqing Key Laboratory of Development and Utilization of Genuine Medicinal Materials in the Three Gorges Reservoir Area,Chongqing 404120,China)
机构地区:[1]重庆三峡医药高等专科学校人体解剖学教研室,重庆404120 [2]三峡库区道地药材开发利用重庆市重点实验室,重庆404120
出 处:《神经解剖学杂志》2022年第3期314-320,共7页Chinese Journal of Neuroanatomy
基 金:重庆市教委科学技术研究项目(KJ1725382);重庆市教委科学技术研究项目(KJQN01802701)。
摘 要:目的:探讨抗沉默功能1B组蛋白伴侣(ASF1B)对人胶质瘤细胞的增殖与侵袭的影响及机制。方法:首先比较GENT2数据库中正常人脑组织与人脑肿瘤组织中ASF1B的表达,分析ASF1B表达与预后的关系;WesternBlot法检测A172、U87、U251和HS683细胞系中ASF1B的表达;采用siRNA技术抑制人脑胶质瘤细胞系U251和U87细胞ASF1B基因表达;分别通过CCK-8法和Transwell小室法检测U251和U87细胞增殖和侵袭情况,Western Blot法检测PI3K/Akt通路中p-Akt和p-mTOR蛋白的表达水平。结果:与正常脑组织相比,ASF1B在人脑肿瘤组织中的表达明显增加,ASF1B高表达的人脑肿瘤患者总生存期更短(P=0.036);ASF1B下调不仅明显抑制U251和U87细胞的增殖和侵袭;也明显抑制p-Akt和p-mTOR蛋白表达。结论:ASF1B通过PI3K/Akt通路促进U251和U87细胞增殖和侵袭。Objective: To investigate the effects and mechanism of anti-silencing function 1 B histone chaperone(ASF1 B) on the proliferation and invasion of human glioma cells. Methods: According to the GENT2 database, the ASF1 B expression in normal human brain tissues and that in human brain cancer tissues were compared, and the relationship between ASF1 B expression and the prognosis of human brain cancer was analyzed. Western Blot assay was used to determine the ASF1 B protein levels in A172, U87, U251, and HS683 cell lines. The siRNA was applied to silence the ASF1 B gene expression in U251 and U87 cells. Cell proliferation and invasion were detected by CCK-8 and Transwell assays respectively, and Western Blot was conducted to detect the expression of the p-Akt and p-mTOR proteins in PI3 K/Akt pathway. Results: The expression of ASF1 B in human brain cancer tissues was significantly increased(P<0.01), compared with that in the normal human brain tissues;Patients with higher ASF1 B expression showed shorter overall survival(P=0.036);The decrease of ASF1 B not only significantly inhibited the proliferation and invasion of the U251 and U87 cells but obviously inhibited the expression of the p-Akt and p-mTOR proteins. Conclusion: ASF1 B promoted the proliferation and invasion of the U251 and U87 cells through the PI3 K/Akt pathway.
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