miR‑338‑3p suppresses tumor growth of ovarian epithelial carcinoma by targeting Runx2
Authors: Chunyan Wen
Hongxi Ma
Wenjie Zhang
Haifeng Li
Xiaojun Liu
Journal: International Journal of Oncology (2015)
Discipline: CLINICAL MEDICINE
Keywords: miR-338-3p; tumorigenesis; metastasis; ovarian epithelial carcinoma; clinicopathological features
Affiliations: Department of Pathology, China-Japan Union Hospital of Jilin University, Nanguan District, Changchun 13033, P.R. China., Department of Obstetrics and Gynecology, China-Japan Union Hospital of Jilin University, Nanguan District, Changchun 13033, P.R. China., Department of Pathology, The First Hospital of Jilin University, Changchun 130021, P.R. China., Department of Emergency Medicine, The First Hospital of Jilin University, Changchun 130021, P.R. China.

Abstract:  miR‑338‑3p, a recently discovered miRNA, has been shown to play important roles in tumorigenesis and metastasis in various cancers. However, the exact roles and mechanisms of miR‑338‑3p remain unknown in human ovarian epithelial carcinoma (EOC). The relationship between miR‑338‑3p expression pattern and clinicopathological features of patients with EOC were determined by real-time quantitative RT-PCR. Furthermore, the role of miR‑338‑3p and possible molecular mechanisms in EOC was investigated by several in vitro approaches and in a nude mouse model. We first showed that the expression of miR‑338‑3p was significantly downregulated in EOC tissues compared to those in adjacent normal tissues, and the value was negatively related to advanced FIGO stage, high histological grading and lymph node metastasis (P&lt;0.01). An in vitro analysis revealed that the overexpression of miR‑338‑3p in EOC cells significantly inhibited cell proliferation, colony formation, migration and invasion, inducing cell apoptosis and enhancing caspase-3, -8, and -9 activities. Bioinformatic analysis and dual luciferase assays identified Runx2 as a direct target of miR‑338‑3p. We also found that enforced expression of miR‑338‑3p markedly inhibited the in vivo tumorigenicity in a nude mouse xenograft model system. Furthermore, overexpression of miR‑338‑3p inhibited phosphorylation of PI3K and AKT, which contributed to suppression of ovarian cancer cell growth. These findings revealed that miR‑338‑3p may act as a tumor suppressor that blocks the growth of human ovarian epithelial carcinoma through PI3K/AKT signaling pathways by targeting Runx2. 

Retracted: Yes

PubPeer comments:
 Fig 4.  (C) Western blot analyses of Runx2 protein expression the ovarian cancer cell lines SKOV3, OVCAR3 and A2780 and human ovarian surface epithelial cell line HOSEpiC. (D) Western blot analysis of Runx2 expression in EOC tissue and corresponding adjacent normal tissue . ![file] Other manifestations of these versatile loading controls include Fig 6 of [Liu et al (2015)] . ![] Fig 6b from [Dong et al (2016)] .  MG63 cells were transfected with E2F3 overexpression plasmid, and the expression of E2F3 on ... protein level (b) was examined by ... western blot . ![file] Fig 5D from [Wang et al (2016)](http: www.ijcem.com files ijcem0017368.pdf),  IRS2 protein expression was determined in four ovarian cancer cell lines (SKOV3, A2780, OVCAR and HO-8910) and human ovarian surface epithelial cell line (HOSEpiC) . ![] *[left]* Fig 5C of [Song et al (2015)] .  Western blotting of EGFR protein expression in the HeLa cells after transfection with the miR-133a mimic or miR-Ctrl. u03b2-actin was used as an internal control. *[right]* Fig 3c from [Zhang et al (2015)] .  The expression levels of MMP-2 and MMP-9 were determined by Western blot after being transfected with miR-133a or miR-NC. GAPDH was used as internal control . ![] Readers may notice some other recurring lanes. , 
 Dear Hoya Camphorifolia, Thank you for your comment. Our team will investigate these questions, and reply you as quickly as possible. Best regards , 
 Retracted [29 June 2021] . ---------------------- Following the publication of this paper, it was drawn to the Editors attention by a concerned reader that the western blotting data shown in Fig. 5C and D bore unexpected similarities to data appearing in different form in other articles by different authors. Owing to the fact that some of the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to *Internatiu03bfnal Journal of Oncology*, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. ,