yuhan hu

Prof. yuhan hu


Research Focus & Metrics

Academic Career Length

10Years (2017-Present)

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

Representative Publications

View All Publications
1 August 2017 in Cellular Signalling
Verified
Journal Article
Closed access
FZFan Zhang
Fan Zhang
YLYan-Xia Lu
Yan-Xia Lu
QCQing Chen
Qing Chen
HZHuimei Zou
Huimei Zou
JZJian-Ming Zhang
Jian-Ming Zhang
XLXue-Nong Li
Xue-Nong Li

3 September 2018 in Cancer Cell International
Verified
Journal Article
Open access
PDF file
YWYongxia Wang
Yongxia Wang
HZHui-Fang Zhu
Hui-Fang Zhu
ZZZhe-Ying Zhang
Zhe-Ying Zhang
FRFeng Ren
Feng Ren
YHyuhan hu
yuhan hu
Growing evidence suggests that MiRNAs play essential roles in the initiation and progression of colorectal cancer (CRC). The aberrant expression of miR-384 has been reported in some cancers. However, the role and mechanism of miR-384 in CRC proliferation remains unknown. The expression of miR-384 was detected in CRC and their paired normal tissues by real-time PCR. In vivo and in vitro assays were conducted to confirm the role of miR-384 in the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro assays were used to confirm that AKT3 was the target gene of miR-384. Finally, Spearman’s correlation analyses was carried out to analyze the relationship between miR-384 expression and AKT3 expression in CRC. MiR-384 was down‑regulated in CRC tissues. The in vivo and vitro functional assays verified that the ectopic upregulation of miR-384 inhibited the proliferation of CRC and the inhibition of miR-384 promoted the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro functional assays confirmed AKT3 as the target gene of miR-384. The expression of miR-384 was negatively correlated with the expressions of AKT3. Our study verified that miR-384 could significantly suppress the proliferation of CRC by directing targeting AKT3.