Hui Fu

Dr. Hui Fu


Research Focus & Metrics

Academic Career Length

18Years (2009-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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18 August 2017 in Oncotarget
Verified
Journal Article
Open access
PDF file
YYYali Yang
Yali Yang
MRMingxin Ren
Mingxin Ren
CSChao Song
Chao Song
DLDan Li
Dan Li
SSShahid Hussain Soomro
Shahid Hussain Soomro
HFHui Fu
Hui Fu
LINC00461, a long non-coding RNA, is important for the proliferation and migration of glioma cells LINC00461, a long non-coding RNA, is important for the proliferation and migration of glioma cells

1 January 2019 in Asian Pacific Journal of Cancer Prevention
Verified
Journal Article
Open access
PDF file
HLHaiwei Lian
Haiwei Lian
MSMin Su
Min Su
YZYijie Zhu
Yijie Zhu
YZYun Zhou
Yun Zhou
SSShahid Hussain Soomro
Shahid Hussain Soomro
HFHui Fu
Hui Fu
The Protein kinase CK2 (formerly known as casein kinase 2) is a highly conserved serine/ threonine kinaseoverexpressed in various human carcinomas and its high expression often correlates with poor prognosis. CK2 proteinis localized in the nucleus of many tumor cells and correlates with clinical features in many cases. Increased expressionof CK2 in mice results in the development of various types of carcinomas (both solids and blood related tumors, suchas (breast carcinoma, lymphoma, etc), which reveals its carcinogenic properties. CK2 plays essential roles in many keybiological processes related to carcinoma, including cell apoptosis, DNA damage responses and cell cycle regulation.CK2 has become a potential anti-carcinoma target. Various CK2 inhibitors have been developed with anti-neoplasticproperties against a variety of carcinomas. Some CK2 inhibitors have showed good results in in vitro and pre-clinicalmodels, and have even entered in clinical trials. This article will review effects of CK2 and its inhibitors on commoncarcinomas in in vitro and pre-clinical studies.

1 April 2021 in Tissue and Cell
Verified
Journal Article
Closed access
MSMin Su
Min Su
SSShahid Hussain Soomro
Shahid Hussain Soomro
JJJifu Jie
Jifu Jie
HFHui Fu
Hui Fu

30 June 2009 in Clinical and Experimental Pharmacology and Physiology
Verified
Journal Article
Closed access
PDF file
LLLihong Long
Lihong Long
RLRui‐Li Liu
Rui‐Li Liu
FWFang Wang
Fang Wang
JLJue Liu
Jue Liu
ZHZhuang‐Li Hu
Zhuang‐Li Hu
JCJian‐Guo Chen
Jian‐Guo Chen

8 January 2024 in Neural Regeneration Research
Verified
Journal Article
Open access
CZChengfu Zhang
Chengfu Zhang
MQMengsheng Qiu
Mengsheng Qiu
HFHui Fu
Hui Fu
Cytokines including tumor necrosis factor, interleukins, interferons, and chemokines are abundantly produced in various diseases. As pleiotropic factors, cytokines are involved in nearly every aspect of cellular functions such as migration, survival, proliferation, and differentiation. Oligodendrocytes are the myelin-forming cells in the central nervous system and play critical roles in the conduction of action potentials, supply of metabolic components for axons, and other functions. Emerging evidence suggests that both oligodendrocytes and oligodendrocyte precursor cells are vulnerable to cytokines released under pathological conditions. This review mainly summarizes the effects of cytokines on oligodendrocyte lineage cells in central nervous system diseases. A comprehensive understanding of the effects of cytokines on oligodendrocyte lineage cells contributes to our understanding of central nervous system diseases and offers insights into treatment strategies.

1 June 2016 in Biochemistry and Cell Biology
Verified
Journal Article
Closed access
RLRuiting Li
Ruiting Li
YLYinghui Li
Yinghui Li
XHXin Hu
Xin Hu
HLHaiwei Lian
Haiwei Lian
LWLei Wang
Lei Wang
HFHui Fu
Hui Fu
Transcription factor 3 (TCF3) is a member of the T-cell factor/lymphoid enhancer factor (TCF/LEF) transcription factor family. Recent studies have demonstrated its potential carcinogenic properties. Here we show that TCF3 was upregulated in glioma tissues compared with normal brain tissues. This upregulation of the TCF3 gene probably has functional significance in brain-tumor progression. Our studies on glioblastoma multiforme (GBM) cell lines show that knock-down of TCF3 induced apoptosis and inhibited cell migration. Further analysis revealed that down-regulation of TCF3 gene expression inhibits Akt and Erk1/2 activation, suggesting that the carcinogenic properties of TCF3 in GBM are partially mediated by the phosphatidylinositol 3-kinase–Akt and MAPK–Erk signaling pathways. Considered together, the results of this study demonstrate that high levels of TCF3 in gliomas potentially promote glioma development through the Akt and Erk pathways.