MicroRNA-19a promotes nasopharyngeal carcinoma by targeting transforming growth factor β receptor 2
Authors: Xianling Liu
Zhiyuan Wang
Chunhong Hu
Jingjing Wang
Fang Ma
Journal: Experimental and Therapeutic Medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: invasion; microRNA; nasopharyngeal carcinoma; proliferation; transforming growth factor β receptor 2.
Affiliations: Department of Oncology, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, P.R. China., Department of Oncology, Tumor Hospital of Hunan, Changsha, Hunan 410013, P.R. China.

Abstract:  MicroRNA (miR), a class of small non-coding RNA, function as key regulators in gene expression through directly binding to the 3' untranslated region of their target mRNA, which further leads to translational repression or mRNA degradation. miR-19a, a member of miR-17-92 cluster, has an oncogenic role in a variety of malignant tumors. However, the exact role of miR-19a in nasopharyngeal carcinoma (NPC) has not previously been studied. The present study aimed to investigate the function and mechanism of miR-19a in regulating the viability and invasion of NPC cells. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) data indicated that the expression levels of miR-17-92 cluster members (miR-17, miR-18a, miR-19a and miR-20a) were frequently increased in NPC tissues compared to the normal tissues. It was also demonstrated that miR-19a was significantly upregulated in NPC C666-1 cells compared to NP69 cells (P&lt;0.01). Knockdown of miR-19a led to a significant decrease in the viability and invasion of NPC C666-1 cells (P&lt;0.01), and induced increased protein expression levels of transforming growth factor β receptor 2 (TGFβR2), which was further identified as a direct target gene of miR-19a by using a luciferase reporter assay. Overexpression of TGFβR2 also suppressed the viability and invasion of C666-1 cells, similar to the effects of miR-19a inhibition. Furthermore, knockdown of TGFβR2 reversed the suppressive effects of miR-19a inhibition on C666-1 cell viability and invasion, suggesting that the role of miR-19a in mediating cell viability and invasion is through directly targeting TGFβR2 in NPC cells. In addition, RT-qPCR data demonstrated that the mRNA expression level of TGFβR2 was markedly reduced in NPC tissues and C666-1 cells. In summary, the present study demonstrated an oncogenic role of miR-19a in NPC via mediation of TGFβR2. Therefore, miR-19a may be a potential therapeutic target for NPC. 

Retracted: Yes

PubPeer comments:
 Fig 2D, 4C.  Transwell assays were used to determine cell ... invasion capabilities . ![file] Colored rectangles indicate overlaps with Fig 4A of [Lei et al (2014)] , ![] and Fig 5A of [Long et al (2016)] . ![file] UPDATE: Figs 3B, 7B of [Zhong et al (2018)] . ![file] Figs 3B, 7B of [Xiao et al (2018)] . ![file] , 
 Retracted [2 August 2021] . ------------------------------ Following the publication of this paper, it was drawn to the Editors attention by a concerned reader that the Transwell cell migration assay data shown in Figs. 2D and 4C 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 *Experimental and Therapeutic Medicine*, 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. ,