Suppr超能文献

CCDC85B 促进非小细胞肺癌细胞的增殖和侵袭。

CCDC85B promotes non-small cell lung cancer cell proliferation and invasion.

机构信息

Department of Pathology, First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, China.

出版信息

Mol Carcinog. 2019 Jan;58(1):126-134. doi: 10.1002/mc.22914. Epub 2018 Oct 9.

Abstract

Coiled-coil domain containing 85 B (CCDC85B) is involved in diverse biological processes; however, its expression patterns and functions in human cancers are yet unknown. The present study demonstrated that the expression of CCDC85B in the cytoplasm of the non-small cell lung cancer (NSCLC) tumor cells was significantly higher compared to adjacent normal lung tissues (P < 0.05). Furthermore, CCDC85B expression correlated with advanced TNM stage (P = 0.004) and positive regional lymph node metastasis (P = 0.009) of NSCLC. In addition, in A549 and H1299 lung cancer cell lines, the overexpression of CCDC85B promoted cell proliferation and invasion, while siRNA-mediated CCDC85B knockdown exhibited opposite effects. CCDC85B promoted AKT and GSK3β phosphorylation and upregulated the levels of active β-catenin, Wnt targets c-myc, cyclin D1, and MMP7. Besides, the CCDC85B-induced upregulation of phosphorylated GSK3β and active β-catenin was rescued following the treatment with PI3 K inhibitor, LY294002. In conclusion, CCDC85B was associated with NSCLC progression as it promoted the proliferation and invasion of lung cancer cells through activated AKT/GSK3β/β-catenin oncogenic signaling pathway. Therefore, CCDC85B might serve as a novel target for NSCLC treatment.

摘要

卷曲螺旋结构域蛋白 85B(CCDC85B)参与多种生物学过程;然而,其在人类癌症中的表达模式和功能尚不清楚。本研究表明,非小细胞肺癌(NSCLC)肿瘤细胞细胞质中 CCDC85B 的表达明显高于相邻正常肺组织(P<0.05)。此外,CCDC85B 的表达与 NSCLC 的晚期 TNM 分期(P=0.004)和阳性区域淋巴结转移(P=0.009)相关。此外,在 A549 和 H1299 肺癌细胞系中,CCDC85B 的过表达促进了细胞增殖和侵袭,而 siRNA 介导的 CCDC85B 敲低则表现出相反的效果。CCDC85B 促进 AKT 和 GSK3β 的磷酸化,并上调活性 β-连环蛋白、Wnt 靶基因 c-myc、周期蛋白 D1 和 MMP7 的水平。此外,在用 PI3K 抑制剂 LY294002 处理后,CCDC85B 诱导的磷酸化 GSK3β 和活性 β-连环蛋白的上调得到挽救。总之,CCDC85B 与 NSCLC 的进展有关,因为它通过激活 AKT/GSK3β/β-连环蛋白致癌信号通路促进肺癌细胞的增殖和侵袭。因此,CCDC85B 可能成为 NSCLC 治疗的新靶点。

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