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4097801 
Journal Article 
MiR-429 induces apoptosis of glioblastoma cell through Bcl-2 
Zhang, Z; Zhou, Q; Miao, Y; Tian, H; Li, Y; Feng, X; Song, X 
2015 
1 
Tumor Biology
ISSN: 1010-4283
EISSN: 1423-0380 
English 
26511969 
WOS:000392941000029 
has retraction 4098513 Retraction Note to multiple articles in Tumor Biology
An essential role of microRNAs (miRNAs) has been acknowledged in the tumorigenesis of glioblastoma multiforme (GBM). Very recently, miR-429 was reported to have a potential of suppressing cancer growth. However, whether miR-429 may similarly regulate growth of GBM remains unknown. Here, we analyzed the levels of miR-429 and anti-apoptotic protein Bcl-2 in GBM specimens. We combined bioinformatics analyses and luciferase reporter assay to determine the relationship between miR-429 and Bcl-2 in GBM cells. Cell survival upon temozolomide treatment was analyzed in a CCK assay. Cell apoptosis was measured by fluorescein isothiocyanate (FITC) Annexin V apoptosis detection assay. We found that miR-429 levels were significantly decreased and Bcl-2 levels were significantly increased in GBM specimens, compared to the paired adjacent non-tumor brain tissue. Moreover, the levels of miR-429 and Bcl-2 inversely correlated. Low-miR-429 subjects had an overall inferior survival, compared to high-miR-429 subjects. MiR-429 targeted the 3'-UTR of Bcl-2 mRNA to inhibit its translation. Overexpression of miR-429 inhibited Bcl-2-mediated cell survival against temozolomide-induced apoptosis, while depletion of miR-429 augmented it. Together, our data suggest that miR-429 suppression in GBM promotes Bcl-2-mediated cancer cell survival against chemotherapy-induced cell death. Re-expression of miR-429 levels in GBM cells may improve the outcome of chemotherapy.