MiR-132 inhibits cell proliferation, invasion and migration of hepatocellular carcinoma by targeting PIK3R3
Authors: Kai Liu
Bo Shi
Jianmeng Wang
Yuchen Cao
Xingliang Li
Yuanyuan Ge
Journal: International Journal of Oncology (2015)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNA-132; tumor suppressive role; hepatocellular carcinoma; target gene; tumor differentiation
Affiliations: Department of Hepatopancreatobiliary Surgery, The First Hospital, Jilin University, Changchun 130021, P.R. China., Department of Internal Medicine Emergency, The First Hospital, Jilin University, Changchun 130021, P.R. China., Department of Clinical Medicine, Bethune Medical School, Jilin University, Changchun 130021, P.R. China., Department of Geriatrics, The First Hospital, Jilin University, Changchun 130021, P.R. China., The Experiment Center, School of Basic Medical Sciences, Jilin University, Changchun 130021, P.R. China.

Abstract:  MicroRNA-132 (miR‑132) has been reported to play a tumor suppressive role in different human malignancies. However, its role and underling mechanism in hepatocellular carcinoma (HCC) remains poorly defined due to lack of target gene information. In the present study, we demonstrated that the mean level of miR‑132 in hepatocellular carcinoma (HCC) tissues was significantly lower than that in matched tumor-adjacent tissues, and its expression negatively correlated with tumor differentiation (P&lt;0.01), TNM stage (P&lt;0.01) and lymph node metastasis (P&lt;0.01). Similarly, the expression of miR‑132 was obviously reduced in HCC cell lines as compared with a normal hepatic cell line. Ectopic expression of miR‑132 inhibited cell proliferation, colony formation, migration and invasion, and induced apoptosis in HepG2 cells. In vivo studies showed that miR‑132 inhibited tumor growth of HCC and decreased tumor volume and weight. In addition, phosphoinositide-3-kinase regulatory subunit 3 (PIK3R3) was identified as a direct target of miR‑132 by a luciferase reporter assay. Western blot and qRT-PCR analysis indicated that PIK3R3 was significantly downregulated by miR‑132 in HCC cells. miR‑132 expression inversely correlated with PIK3R3 mRNA expression in clinical HCC tissues. Investigations into possible mechanisms revealed that miR‑132 inactivated the AKT/mTOR signaling pathway, which may contribute to inhibition of proliferation, migration, and invasion of HCC. These findings suggested that miR‑132 may serve as a potential target in the treatment of human HCC. 

Retracted: Yes

PubPeer comments:
 *[above]* Fig 2C.  Cell colony formation was determined in HepG2 cells transfected with miR-132 mimic or miR-control. *[below]* Fig 6D from [Wang et al (2017)] .  colony formation... determined in SKOV3 cells transfected with miR-365 or miR-Ctrl and with or without Wnt5a overexpression plasmid . ![file] How to explain the coincidence? , 
 *[above]* Fig 3A.  Cell cycle was analyzed by FACS in HepG2 cells transfected with miR-132 mimic or miR-control. *[below]* Fig 4A from [Jin et al (2015)] .  Cell cycle ... determined by flow cytometry in MDA-MB-231 cells after transfection with miR-338-3p mimic and determined with wound healing assay [??] Surprisingly similar. ![file] , 
 Retracted [29 June 2021] . ------------------------------------------ Following the publication of this paper, it was drawn to the Editors attention by a concerned reader that the data shown in Figs. 2C and 3A 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 *International 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. ,