Suppr超能文献

IL-6 上调 CCDC68 促进子宫内膜癌进展。

CCDC68 Upregulation by IL-6 Promotes Endometrial Carcinoma Progression.

机构信息

The First Affiliated Hospital of Anhui Medical University, Hefei, China.

出版信息

J Interferon Cytokine Res. 2021 Jan;41(1):12-19. doi: 10.1089/jir.2020.0193.

Abstract

The elevation of circulating interleukin 6 (IL-6) is one of the major molecular characteristics of endometrial carcinoma. In this study, we investigated the role of coiled-coil domain-containing 68 (CCDC68) in IL-6-associated endometrial carcinoma progression. CCDC68 expression levels and the activation of IL-6 pathway were detected by qPCR and Western blot. Stable CCDC68 knockdown Ishikawa and RL-95 cells were created to investigate cancer cell proliferation, migration, and invasion with or without IL-6 administration. Kaplan-Meier's analysis was used to determine the correlation between CCDC68 expression and overall survival or recurrence-free survival in endometrial carcinoma patients. CCDC68 expression level is significantly uregulated by IL-6 stimulation. Increased CCDC68 expression predicts poor prognosis in endometrial carcinoma patients. CCDC68 knockdown dramatically inhibit IL-6-associated cancer cell proliferation, migration, invasion, and downregulate the expression of proto-oncogenes in endometrial carcinoma cells. CCDC68 acts as a cancer-promoting factor in IL-6-stimulated endometrial carcinoma cells, and blocking the expression of CCDC68 might be a novel therapeutic strategy for the endometrial carcinoma treatment.

摘要

循环白细胞介素 6(IL-6)水平升高是子宫内膜癌的主要分子特征之一。在本研究中,我们研究了卷曲螺旋结构域包含蛋白 68(CCDC68)在 IL-6 相关子宫内膜癌进展中的作用。通过 qPCR 和 Western blot 检测 CCDC68 表达水平和 IL-6 通路的激活情况。创建了稳定敲低 CCDC68 的 Ishikawa 和 RL-95 细胞,以研究在有或没有 IL-6 给药的情况下癌细胞增殖、迁移和侵袭的情况。Kaplan-Meier 分析用于确定 CCDC68 表达与子宫内膜癌患者总生存期或无复发生存期之间的相关性。IL-6 刺激显著上调 CCDC68 表达水平。CCDC68 表达水平升高预示着子宫内膜癌患者预后不良。CCDC68 敲低显著抑制 IL-6 相关的癌细胞增殖、迁移、侵袭,并下调子宫内膜癌细胞中原癌基因的表达。CCDC68 作为 IL-6 刺激的子宫内膜癌细胞中的促癌因子,阻断 CCDC68 的表达可能是子宫内膜癌治疗的一种新的治疗策略。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验