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1.
Mol Med Rep ; 24(3)2021 Sep.
Article in English | MEDLINE | ID: mdl-34278475

ABSTRACT

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the cell apoptosis assay data shown in Figs. 1C and 4D were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 12: 3923­3929, 2015; DOI: 10.3892/mmr.2015.3826].

2.
Mol Med Rep ; 12(3): 3923-3929, 2015 Sep.
Article in English | MEDLINE | ID: mdl-26004124

ABSTRACT

MicroRNAs (miRs) are a class of non-coding RNAs that function as key regulators of gene expression at the post-transcriptional level. miR-148a has been suggested to be associated with human ovarian cancer, however, the detailed functions of miR­148a in ovarian cancer remain to be fully elucidated. The present study aimed to investigate the regulatory mechanism of miR-148a in ovarian cancer cells. Reverse transcription­quantitative polymerase chain reaction and western blot analysis were conducted to examine the RNA and protein levels, respectively. The luciferase reporter assay was used to determine the target relationship. Cell proliferation and apoptosis assays were additionally conducted. The present study demonstrated that miR­148a inhibited cell proliferation and promoted the paclitaxel­induced apoptosis of ovarian cancer cells. Furthermore, protein disulfide isomerase family A, member 3 (PDIA3) was identified as a target gene of miR­148a. A fluorescent reporter assay was performed to confirm that miR­148a was able to directly bind to the 3'­untranslated region of PDIA3 mRNA. In addition, miR­148a was frequently downregulated in ovarian cancer tissue, whereas the expression levels of PDIA3 were increased. Knockdown of PDIA3 significantly inhibited the proliferation and promoted the paclitaxel­induced apoptosis of the ovarian cancer cells, whereas overexpression of PDIA3 had the opposite effects. Therefore, the results of the present study suggested that miR­148a inhibited the proliferation and promoted the paclitaxel­induced apoptosis of ovarian cancer cells, and this may be partly attributed to direct targeting of PDIA3.


Subject(s)
Antineoplastic Agents, Phytogenic/pharmacology , Cell Proliferation , MicroRNAs/genetics , Ovarian Neoplasms/metabolism , Paclitaxel/pharmacology , Protein Disulfide-Isomerases/genetics , 3' Untranslated Regions , Apoptosis , Base Sequence , Binding Sites , Cell Line, Tumor , Female , Gene Expression Regulation, Neoplastic/drug effects , Humans , Ovarian Neoplasms/drug therapy , Ovarian Neoplasms/pathology , Protein Disulfide-Isomerases/metabolism , RNA Interference
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