MicroRNA-148a inhibits the proliferation and promotes the paclitaxel-induced apoptosis of ovarian cancer cells by targeting PDIA3
Authors: Shanshan Liu
Zhengfang Wen
Shaoru Li
Ying Liu
Shuzhen Zhao
Xiaorui Li
Yanna Ge
Journal: Molecular Medicine Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNAs; miR-148a; ovarian cancer; gene expression; post-transcriptional level
Affiliations: Department of Gynecology and Obstetrics, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan 453100, P.R. China., Department of Oncology, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan 453100, P.R. China.

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 miR‑148a 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 transcription‑quantitative 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 miR‑148a inhibited cell proliferation and promoted the paclitaxel‑induced apoptosis of ovarian cancer cells. Furthermore, protein disulfide isomerase family A, member 3 (PDIA3) was identified as a target gene of miR‑148a. A fluorescent reporter assay was performed to confirm that miR‑148a was able to directly bind to the 3'‑untranslated region of PDIA3 mRNA. In addition, miR‑148a 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 paclitaxel‑induced apoptosis of the ovarian cancer cells, whereas overexpression of PDIA3 had the opposite effects. Therefore, the results of the present study suggested that miR‑148a inhibited the proliferation and promoted the paclitaxel‑induced apoptosis of ovarian cancer cells, and this may be partly attributed to direct targeting of PDIA3. 

Retracted: Yes

PubPeer comments:
 Figs 1C, 4D.  Overexpression of miR-148a promoted paclitaxel-induced cell apoptosis, whereas inhibition of miR-148a suppressed paclitaxel-induced cell apoptosis, compared with the control group ;  Overexpression of PDIA3 inhibited paclitaxel-induced cell apoptosis, whereas inhibition of PDIA3 promoted paclitaxel-induced cell apoptosis, compared with the control . ![file] Control and NC panels are the same. The same panels have appeared in other papers: Figs 2C; 4B from [He, Tang Tian (2015)] .  A cell apoptosis assay was performed to examine the cell proliferation of CNE1 cells transfected with miR-214 mimics or the miR-214 inhibitor ;  A cell apoptosis assay was performed to determine the apoptotic rate of CNE1 cells transfected with the miR-214 inhibitor or co-transfected with the miR-214 inhibitor and Bax siRNA . ![file] *[above]* Fig 4A from [Peng et al (2013)] .  Flow cytometry was used to determine the apoptotic rate of U87 and CHG-5 cells after forced downregulation of RACK1.  *[below[* Fig 4B from [Lai, Chen Li (2015)] .  ... a Transwell assay were performed to examine the cell proliferation of AGS cells transfected with miR-133a mimics, miR-133a inhibitor, or co-transfected with miR-133a mimics and FSCN1 plasmid. Control: AGS cells without any transfection. ![file] , 
 #1 Figs 1C, 4D again. Another panel color-coded: ![file] ...to match Fig 2D of [Liu et al (2016)] . ![file] , 
 Retracted [14 July 2021] . ------------------------------------ Following the publication of this paper, it was drawn to the Editorsu2019 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. ,