RESUMO
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell invasion assay data shown in Fig. 3A and B on p. 1306 were strikingly similar to data appearing in different form in a paper by different authors at a different research institute that had already been submitted for publication. Owing to the fact that the contentious data in the above article had already been submitted for publication prior to its submission to International Journal of Molecular Medicine, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 46: 13011310, 2020; DOI: 10.3892/ijmm.2020.4704].
RESUMO
MicroRNAs (miRNAs) have been reported to have important regulatory roles in the progression of several types of cancer, including cervical cancer (CC). However, the biological roles and regulatory mechanisms of miRNAs in CC remain to be fully elucidated. The aim of the present study was to examine the functions of miRNAs in CC and the possible mechanisms. Using a microarray, it was identified that miRNA15a5p (miR15a5p) was one of the most downregulated miRNAs in CC tissues compared with adjacent noncancerous tissues. The low expression of miR15a5p was observed in CC tumor tissues with distant metastasis and in CC cell lines. In addition, the effects of miR15a5p upregulation on cell viability, apoptosis, invasion and migration of CC cells were investigated using CCK8, flow cytometry, Transwell and wound healing assays, respectively. It was demonstrated that upregulation of miR15a5p significantly suppressed the viability, migration and invasion, and promoted the apoptosis of SiHa and C33A cells. Furthermore, yesassociated protein 1 (YAP1), a wellknown oncogene, was confirmed to be directly targeted by miR15a5p and was found to be negatively regulated by miR15a5p. Further correlation analysis indicated that miR15a5p expression was negatively correlated with YAP1 expression in CC tissues. Notably, overexpression of YAP1 abrogated the tumor suppressive effects of miR15a5p in CC cells. Taken together, these present findings indicated that the miR15a5p/YAP1 axis may provide a novel strategy for the clinical treatment of CC.