MiR-218-5p inhibits the stem cell properties and invasive ability of the A2B5‚Å∫CD133‚Å?subgroup of human glioma stem cells
Authors: Youxin Zhou
Zhiwu Wu
Guilin Chen
Ziwei Du
Yanyan Li
Yulun Huang
Xuetao Li
Ting Sun
Yong Han
Journal: Oncology Reports (2016)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNAs; oncogenes; tumor-suppressor genes; proliferation; apoptosis
Affiliations: Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.

Abstract:  MicroRNAs (miRs) act as oncogenes or tumor-suppressor genes, and regulate the proliferation, apoptosis, invasion, differentiation, angiogenesis and behavior of glioma stem cells, which are important in glioma development and recurrence. The present study was performed to investigate the impact of miR-218-5p on stem cell properties and invasive ability of the A2B5+CD133- human glioma stem cell subgroup. qRT-PCR was used to detect miR-218-5p expression in non-cancerous brain and human glioma tissues, human glioma cell lines and human glioma stem cell lines. Lentivirus vectors encoding miR-218-5p and anti-miR-218-5p were constructed and stably transfected into A2B5+CD133- SHG-139s cells. Neurosphere formation Cell Counting Kit-8 (CCK-8) and Transwell assays, immunofluorescence and qRT-PCR analyses were used to explore the role of miR-218-5p in SHG-139s cells. qRT-PCR analysis showed that miR-218-5p expression was lower in human glioma tissues and cells than in non-cancerous brain tissues and normal human astrocyte cells, and lower in A2B5+CD133- (SHG-139s) cells than in CD133+ (SU2 and U87s) cells. The CCK-8 assay demonstrated that the growth curve was significantly inhibited in the miR-218-5p-SHG-139s cells compared to the miR-control, blank and anti-miR‚Ä?18-5p groups. The neurosphere formation assay indicated that upregulation of miR‚Ä?18-5p expression inhibited SHG-139s neurosphere formation. Immunofluorescence staining and qRT-PCR showed that miR-218-5p reduced stem cell marker (A2B5, nestin, PLAGL2, ALDH1 and Sox2) expression compared with the controls; however, immunofluorescence staining analysis showed that upregulation of miR-218-5p expression led to no difference in CD133 expression. miR‚Ä?18-5p reduced SHG-139s cell invasiveness in the Transwell assay and reduced MMP9 expression as detected in qRT-PCR and immunofluorescence analyses. All differences were statistically significant. miR-218-5p expression was lower in human glioma tissues, cells and the A2B5+CD133- human glioma stem cell subgroup. miR-218-5p may be a tumor-suppressor gene in glioma that functions by upregulating miR-218-5p expression, which inhibits the stem cell properties and invasive properties of SHG-139s cells. 

Retracted: No

PubPeer comments:
 Figure 5. * Boxes of the same color highlight DAPI panels that look more similar then expected, with the similarities also present in the second and Merge columns, which is even more unexpected. * Of particular note, the similarities in the panels marked with cyan boxes is only partial.  , 
 Figure 6. * Orange boxes: The  blank and  miR-control panel appear to overlap.  , 
 Retracted, [1 August 2022] .  Following the publication of this paper, it was drawn to the Editors attention by a concerned reader that Fig. 5 on p. 874 contained a series of DAPI panels within the figure that looked unexpectedly similar in appearance, with the similarities also evident in the second and u2018Mergeu2019 data columns; moreover, of especial note, the similarities in the u2018DAPIu2019 panels for the Blank control experiments shown in Fig. 5C and D only affected a partial section of the data. In addition, the u2018blanku2019 and u2018miRu2011controlu2019 panels in Fig. 6A also appeared to contain overlapping data. Independently of the issues that were raised by the interested reader, the authors themselves requested that their paper be retracted on account of having identified some problems with the presentation of various of the figures, and no longer being able to access their original data. The Editor of Oncology Reports has agreed that this paper should be retracted from the Journal, and apologizes to the readership for any inconvenience caused. ,