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CCDC68 Upregulation by IL-6 Promotes Endometrial Carcinoma Progression
Journal of Interferon & Cytokine Research ( IF 1.9 ) Pub Date : 2021-01-18 , DOI: 10.1089/jir.2020.0193
Xuqing Li 1 , Hongyan Li 1 , Xueting Pei 1 , Youwei Zhou 1 , Zhaolian Wei 1
Affiliation  

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.

中文翻译:

IL-6 上调 CCDC68 促进子宫内膜癌进展

循环白细胞介素 6 (IL-6) 的升高是子宫内膜癌的主要分子特征之一。在这项研究中,我们研究了包含卷曲螺旋结构域的 68 (CCDC68) 在 IL-6 相关子宫内膜癌进展中的作用。通过qPCR和Western印迹检测CCDC68表达水平和IL-6通路的激活。创建稳定的 CCDC68 敲低 Ishikawa 和 RL-95 细胞,以研究使用或不使用 IL-6 的癌细胞增殖、迁移和侵袭。Kaplan-Meier 的分析用于确定 CCDC68 表达与子宫内膜癌患者的总生存期或无复发生存期之间的相关性。CCDC68 表达水平受 IL-6 刺激显着调节。CCDC68 表达增加预示子宫内膜癌患者预后不良。CCDC68 敲低可显着抑制 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 在 IL-6 刺激的子宫内膜癌细胞中充当促癌因子,阻断 CCDC68 的表达可能是子宫内膜癌治疗的新治疗策略。
更新日期:2021-01-21
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