标题:CUL4B regulates autophagy via JNK signaling in diffuse large B-cell lymphoma
作者:Li, Ying; Zhou, Xiangxiang; Zhang, Ya; Yang, Juan; Xu, Yangyang; Zhao, Yi; Wang, Xin
作者机构:[Li, Ying; Zhou, Xiangxiang; Zhang, Ya; Yang, Juan; Xu, Yangyang; Zhao, Yi; Wang, Xin] Shandong Univ, Shandong Prov Hosp, Dept Hematol, Jinan, Shandon 更多
通讯作者:Wang, X;Wang, X
通讯作者地址:[Wang, X]Shandong Univ, Shandong Prov Hosp, Dept Hematol, Jinan, Shandong, Peoples R China;[Wang, X]Shandong Univ, Sch Med, Jinan, Shandong, Peoples R 更多
来源:CELL CYCLE
出版年:2019
卷:18
期:4
页码:379-394
DOI:10.1080/15384101.2018.1560718
关键词:Cullin4b; diffuse large B-cell lymphoma; cell proliferation; autophagy;; signaling pathway
摘要:Aberrant expression of CUL4B was identified in various types of solid cancers. Cumulative evidences support the oncogenic role of CUL4B in cancers, including regulation of cell proliferation and signal transduction. However, its clinical value and potential pathogenic mechanism in diffuse large B-cell lymphoma (DLBCL) have not been described previously. Therefore, we hypothesize that overexpressed CUL4B may contribute to the pathogenesis of DLBCL. The aim of this study is to assess the expression and the biological function of CUL4B in DLBCL progression. In our study, CUL4B overexpression was observed in DLBCL tissues, and its upregulation was closely associated with poor prognosis in patients. Furthermore, the functional roles of CUL4B was detected both in vitro and in vivo. We demonstrated that silencing CUL4B could not only induce cell proliferation inhibition, cell cycle arrest, and motility attenuation of DLBCL cells in vitro, but also decrease tumor growth in DLBCL xenografts mice. In addition, we identi?ed that CUL4B may act as a potent inductor of JNK phosphorylation in regulation of autophagy. Our findings demonstrated a significant role of CUL4B in the development and progression of DLBCL. CUL4B may act as a useful biomarker and a novel therapeutic target in DLBCL.
收录类别:SCOPUS;SCIE
WOS核心被引频次:1
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-85060940767&doi=10.1080%2f15384101.2018.1560718&partnerID=40&md5=70a30fdc632baefd621c773bbee28a51
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