MicroRNA-181 inhibits the proliferation, drug sensitivity and invasion of human glioma cells by targeting Selenoprotein K (SELK)
Authors: Yue Liu
Chun-Hua Xu
Dong-Hai Li
Er-Ming Zeng
Li-Ke Chen
Su-Yue Zheng
Li-Min Xiao
Journal: American journal of translational research (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Glioma; MicroRNA; SELK; cell cycle arrest; invasion
Affiliations: Department of Neurosurgery, The First Affiliated Hospital of Nanchang University Nanchang 330006, China.

Abstract:  Gliomas are aggressive type of brain tumors and cause significant human mortality world over. The frequent relapses, development of drug resistance, the adverse effects of the chemotherapy and dearth of the therapeutic targets form the major hurdles in glioma treatment. Several studies suggest that microRNAs (miRs) are involved in the development and progression of different cancers. Herein, the therapeutic potential of miR-181 was explored in human glioma cells. The results showed that miR-181 is significantly downregulated in human glioma cells. Overexpression of miR-181 caused significant inhibition in the proliferation of U87 and U118 glioma cells. The miR-181 triggered growth inhibition was found to be mainly due to the induction of apoptosis which was concomitant with increase in the Bax/Bcl-2 ratio. Additionally, miR-181 enhanced the chemosensitivity of the glioma cells to temozolomide and suppressed their invasion. Bioinformatic analysis showed that miR-181 exerts its effects by inhibiting the expression of Selenoprotein K (SELK). The expression of SELK was found to be significantly upregulated in glioma cells and silencing of SELK suppressed the proliferation of glioma cells. Nonetheless, overexpression of SELK could nullify the effects of miR-181 on the proliferation of the glioma cells. Taken together, miR-181 may exhibit therapeutic implications in the treatment of glioma. 

Retracted: No

PubPeer comments:
 Figure 3B.  miR-181 induces apoptosis in glioma cells. ...  (B) annexin V PI staining of miR-NC and miR-181 mimics transfected U87 and U118 cells showing induction of apoptosis. ![file] For comparison: *[left]* Figure 6 from [Liu et al (2019)] .  Annexin V PI assay showing percentage of apoptotic MDA-MB-231 cells at indicated concentrations of withaferin-A. *[right]* Fig. 2b from [Li et al (2020)] .  Annexin V PI staining showing the percentage of apoptotic U87 and U118 cells . ![file] , 
 *[below]* Figure 5 from [Xu et al (2019)] .  Transwell assay showing the effect of miR-181 overexpression on the invasion of U87 and U118 cells. *[above]* Figure 6 from [Lu et al (2019)] .  Transwell assay showing the cell invasion in NC and miR-15 mimics transfected MDA-T32 cells . ![file] , 
 *[right]* Figure 2 from [Xu et al (2019)] .  Colony formation assay showing the colon formation in miR-NC and miR-181 mimics transfected U87 and U118 cells. *[left]* Figure 2 from [Liu et al (2020)] .  Effect of on the colony formation of the psilostachyin-A treated HepG2 cells as determined by microscopy. ... Psilostachyin-A decreased cancer colony formation dose-dependently. ![file] , 
 #1 *[right]* Figure 3A,B from [Xu et al (2019)] .  miR-181 induces apoptosis in glioma cells. (A) DAPI staining and (B) annexin V PI staining of miR-NC and miR-181 mimics transfected U87 and U118 cells showing induction of apoptosis . *[left]* Fig 1E from [Zhang et al (2020)] .  Suppression of miR-1179 inhibits proliferation of ovarian cancer cell lines ... DAPI, AO EB or annexin V PI staining of NC or miR-1179 inhibitor transfected ... SK-OV-3 . ![file] , 
 Corrected [15 August 2021] .  Readers have raised some concerns about this article. Therefore, we repeated our experiments, and the images for Figures 2, u200b,3A,3A, u200b,3B3B and u200band55 were replaced. The figure legends are correct, and, as such, there are no changes. These changes have no bearing on the studyu2019s conclusions. We would like to publish this erratum to reflect this change. The authors express their regrets for this mistake. ,