[1]刘静雅,张海亮,李宝平,等.长链非编码 RNA SNHG1在子宫内膜癌中的表达及调控 PI3K/AKT信号通路的研究[J].现代检验医学杂志,2022,37(01):119-124.[doi:10.3969/j.issn.1671-7414.2022.01.024]
 LIU Jing-ya,ZHANG Hai-liang,LI Bao-ping,et al.Expression of Long Non-coding RNA SNHG1 in Endometrial Carcinoma and Its Regulation of PI3K/AKT Signaling Pathway[J].Journal of Modern Laboratory Medicine,2022,37(01):119-124.[doi:10.3969/j.issn.1671-7414.2022.01.024]
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长链非编码 RNA SNHG1在子宫内膜癌中的表达及调控 PI3K/AKT信号通路的研究()
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《现代检验医学杂志》[ISSN:/CN:]

卷:
第37卷
期数:
2022年01期
页码:
119-124
栏目:
论 著
出版日期:
2022-01-15

文章信息/Info

Title:
Expression of Long Non-coding RNA SNHG1 in Endometrial Carcinoma and Its Regulation of PI3K/AKT Signaling Pathway
文章编号:
1671-7414(2022)01-119-06
作者:
刘静雅张海亮李宝平李 冲郭初阳
(咸阳市中心医院病理科,陕西咸阳 712000)
Author(s):
LIU Jing-yaZHANG Hai-liangLI Bao-pingLI ChongGUO Chu-yang
(Department of Pathology, Xianyang Central Hospital,Shaanxi Xianyang 712000,China)
关键词:
子宫内膜癌长链非编码 RNA小核仁 RNA宿主基因 1增殖转移细胞周期
分类号:
R737.33;R730.43
DOI:
10.3969/j.issn.1671-7414.2022.01.024
文献标志码:
A
摘要:
目的 研究长链非编码 RNA小核仁 RNA宿主基因 1(lncRNA SNHG1)在子宫内膜癌组织中的表达及临床意义,并探讨 SNHG1在子宫内膜癌中的生物学功能。方法 应用实时荧光定量 PCR(qRT-PCR)检测 SNHG1在 54例子宫内膜癌组织和癌旁组织中的表达水平,并分析子宫内膜癌组织中 SNHG1的表达水平与患者临床病理参数的关系以及其对子宫内膜癌患者预后的影响。 SNHG1 小干扰 RNA(siRNA)转染子宫内膜癌细胞系 Ishikawa,分为 si-NC组和 si-SNHG1组,应用 qRT-PCR检测 SNHG1 siRNA转染效果。干扰 SNHG1 的表达后,采用 MTS实验检测细胞的增殖活性,流式细胞仪检测细胞周期情况,Transwell实验检测细胞的转移能力,western blotting检测细胞中 PI3K/AKT信号通路激活情况, Logrank法比较 SNHG1高低表达人群的生存率差异。结果 SNHG1在子宫内膜癌组织中的表达高于癌旁组织(t=5.236,P=0.000),其高表达与 FLGO分期、肌层浸润深度和淋巴结转移有关( t=2.289~3.136,P=0.003~0.037),且高表达 SNHG1的子宫内膜癌患者生存率较低( χ2=33.266,P=0.000),差异均有统计学意义。抑制 SNHG1表达后, Ishikawa细胞的增殖和转移能力下降,细胞阻滞在 G0/G1期,细胞中 pPI3K和 pAKT蛋白的表达减少。结论 SNHG1在子宫内膜癌中表达上调,且其高表达水平与不良病理参数相关。干扰 SNHG1可抑制子宫内膜癌的增殖和转移, SNHG1可能是通过调节 PI3K/AKT信号通路参与子宫内膜癌的发生、发展。
Abstract:
Objective To investigate the expression and clinical significance of long non-coding RNA small nucleolar RNA hostgene 1 (lncRNA SNHG1) in endometrial carcinoma, and to explore the biological function of SNHG1 in endometrial carcinoma.Methods Real-time fluorescent quantitative PCR (qRT-PCR) was used to detect the expression level of SNHG1 in 54 casesof endometrial carcinoma and adjacent tissues, and the relationship between the expression level of SNHG1 in endometrialcarcinoma and the clinicopathological parameters and its influence on the prognosis of endometrial carcinoma were analyzed.SNHG1 small-interfering RNA(siRNA) was transfected into the endometrial cancer cell line Ishikawa, which was divided intosi-NC group and si-SNHG1 group. QRT-PCR was used to detect the effect of SNHG1 siRNA transfection. After interfering withthe expression of SNHG1, the proliferation activity of the cells was detected by MTS assay, the cell cycle was detected by flowcytometry, the metastasis ability of the cells was detected by Transwell assay, and the activation of PI3K/AKT signaling pathwaywas detected by western blotting, the survival rate of population with SNHG1 high and low expression was compared. Results Theexpression of SNHG1 in endometrial carcinoma tissues was higher than that in adjacent tissues (t=5.236, P=0.000),the highSNHG1 expression was related to FLGO stage, depth of myometrial invasion and and lymph node metastasis (t=2.289~3.136,P=0.003~0.037), and the survival rate of endometrial carcinoma patients with high expression of SNHG1 was lower (χ2=33.266,P=0.000), the differences were statistically significant, respectively. Inhibition of snhg1 expression decreased the proliferationand metastasis of Ishikawa cells, and the cell arrest was induced in the G0/G1 phase, and the expression of pPI3K and pAKTprotein were decreased in the cells. Conclusion The expression of SNHG1 was up-regulated in endometrial carcinoma, and itshigh expression level was related to adverse pathological parameters. Interference with SNHG1 can inhibit the proliferation andmetastasis of endometrial carcinoma. SNHG1 may be involved in the occurrence and development of endometrial carcinoma byregulating PI3K/Akt signal pathway.

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备注/Memo

备注/Memo:
作者简介:刘静雅(1984-),女,本科,主治医师,研究方向:妇产科肿瘤病理学诊断, E-mail:liujingya19840727@163.com。
更新日期/Last Update: 1900-01-01