miR-96/HBP1/Wnt/β-catenin regulatory circuitry promotes glioma growth
Authors: Zhiyong Yan
Weiguo Qi
Jianpeng Wang
Shusheng Che
Yingbing Jiao
Chao Wang
Journal: FEBS Letters (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Glioma; HMG-box transcription factor 1; Proliferation; Wnt/β-catenin; miR-96.
Affiliations: Department of Neurosurgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China., Department of Neurosurgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China. Electronic address: .

Abstract:  We found that miR-96 is overexpressed in glioma, and its level inversely correlates with the survival of patients. The reduction in miR-96 abundance suppresses the proliferation and colony formation of glioma cells. The tumorigenicity of U-87 MG cells is reduced by miR-96 silencing. miR-96 contributes to the activation of Wnt/β-catenin pathway in glioma cells. HMG-box transcription factor 1 (HBP-1), a Wnt/β-catenin pathway inhibitor, is suppressed by miR-96. The reactivation of Wnt/β-catenin signaling causes an increase in the proliferation of glioma cells, and a decrease in miR-96 expression. On the other hand, HBP1 silencing promotes miR-96 expression. Collectively, miR-96 contributes to the progression of glioma by enhancing the activation of the Wnt/β-catenin pathway, and the miR-96/HBP1/Wnt/β-catenin regulatory circuitry promotes the proliferation of glioma cells. 

Retracted: Yes

PubPeer comments:
 Fig 4C.  Immunoblot analysis of phosphorylated and nuclear b-catenin was performed in U-87 MG and U-251 MG cells transfected with miR-96 inhibitors for 48 h. ![file] It is a versatile loading control. [left] Figs 5B,C from [Kong et al (2016)] .  The expression level of HBP1 was detected by immunoblot analysis in U2OS and SaOS2 cells treated with miR-155 inhibitor ;  The expression level of HBP1 was detected by immunoblot analysis in hFOB1.19 and HEK293 cells transfected with miR-155 mimics . *[right]* Fig 7A from [Hong et al (2015)] .  A549 cells were infected with Ad-piR-55490 or and Ad-mTOR (10 MOI) as well as Ad-EGFP (10 MOI), and 48 h later, immunoblot analysis was performed to detect mTOR expression level . ![] , 
 Fig 2A.  U-87 MG cells were treated with miR-96 inhibitor plus HBP1 siRNA (siHBP1) or siHBP1alone. 48 h later, HBP1 expression was detected by immunoblot assays . ![file] Other manifestations of the loading control include *[left]* Fig 5E. from [Zhang, Zhang Li (2016)] .  MEF2D protein was examined by immunoblotting in A549 and H460 cells under such treatments . *[right]* Fig 4B from [Hong et al (2015)] .  Western blot assay was conducted to confirm the above results . ![] Fig 2C from [Cao et al (2015)] .  Cardiac myxoma cells were transfected with MEF2D siRNA or control (50 nM). Twenty-four hours later, MEF2A, MEF2C and MEF2D proteins were determined by immunoblot analysis. ![file] , 
 Retracted [1 March 2022] .  The above article from FEBS Letters, published online on 12 June 2014 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal s Editor-in-Chief, Michael Brunner, the FEBS Press and John Wiley Sons Ltd. The retraction has been agreed due to concerns raised about Figures 4C, 6A and 6C. There is evidence of image manipulation and the duplication of image elements from four subsequently published articles. The authors and the authors institution failed to reply to the journal s requests to provide original data confirming that the images arose from the reported experiments are genuine, unmodified and suitable for publication. ,