Long noncoding RNA SNHG14 promotes�the�aggressiveness of retinoblastoma by sponging microRNA‑124 and thereby upregulating STAT3
Authors: Jing Gao
Shubin Liu
Shuyan Zhang
Xiaowen Sun
Hui Shen
Journal: International Journal of Molecular Medicine (2020)
Discipline: CLINICAL MEDICINE
Keywords: SNHG14; retinoblastoma; miR-124; STAT3; ceRNA
Affiliations: Department of Ophthalmology, People's Hospital of Rizhao, Rizhao, Shandong 276800, P.R. China., Department of Oncology, Binzhou People's Hospital, Binzhou, Shandong 256610, P.R. China., Department of Ophthalmology, Weifang Ophthalmic Hospital, Weifang, Shandong 261041, P.R. China.

Abstract:  A long noncoding RNA called small nucleolar RNA host gene 14 (SNHG14) has been validated as a key regulator of cellular processes in multiple types of human cancer. However, to the best of our knowledge, the expression status and specific roles of SNHG14 in retinoblastoma (RB) have not been studied. The aims of the present study were to determine the expression status of SNHG14 in RB, assess the effects of SNHG14 on malignant characteristics of RB cells and investigate the mechanisms of action of SNHG14 in RB. SNHG14 expression levels in RB tissue samples and cell lines were measured by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Cell proliferation, apoptosis, migration and invasion in vitro, and tumor growth in vivo were quantitated by the Cell Counting Kit‑8 assay, flow cytometry, migration and invasion assays, and mouse tumor xenograft experiments, respectively. The target microRNA (miRNA) of SNHG14 was predicted by bioinformatics analysis and was subsequently validated by a luciferase reporter assay, RNA immunoprecipitation (RIP) assay, RT‑qPCR, and western blot analysis. SNHG14 was identified to be significantly overexpressed in RB tissues and cell lines. SNHG14 overexpression was markedly associated with the intraocular international retinoblastoma classification stage, optic nerve invasion, and differentiation grade among patients with RB. The patients in the SNHG14 high‑expression group exhibited shorter overall survival compared with the SNHG14 low‑expression group. Functional analysis revealed that SNHG14 silencing inhibited cell proliferation, migration and invasion, and increased apoptosis in vitro, and decreased tumor growth in vivo. SNHG14 directly interacted with, and functioned as a competing endogenous RNA (ceRNA) of, miR‑124, consequently upregulating signal transducer and activator of transcription 3 (STAT3). miR‑124 inhibition and STAT3 expression recovery attenuated the effects of the SNHG14 silencing on RB cells. In conclusion, SNHG14 served as a ceRNA to upregulate STAT3 by sponging miR‑124. Therefore, targeting the SNHG14/miR‑124/STAT3 pathway may be an effective therapeutic strategy against RB. 

Retracted: Yes

PubPeer comments:
 *[right]* Fig 6A.  Representative images of tumor xenografts following subcutaneous injection of Y79 cells transfected with either si-SNHG14 or si-NC . *[left]* Fig 9A from [Li et al (2019)] .  Representative images of tumor xenografts obtained from mice injected with si-TINCR- and si-NC-transfected EOC cells . ![file] Surprisingly similar. , 
 Two flow-cytometry plots share most of their points in common, and appear to be derived from the same experiment, with slight differences in gating and filtering. I have adjusted the aspect and contrast to facilitate comparison. ![file] The right-hand panel is from Figs 2C, 4D, 5C. The left-hand panel is from Figs 2C, 4B, 5C, 6E of [Wu et al (2019)] . Here in context: ![file] ![] There may be other matching panels. The low resolution is regrettable; perhaps the publishers have limited storage resources for large files. , 
 Retracted [23 March 2022] .  Following the publication of the above paper, it was drawn to the Editors attention by a concerned reader that certain of the tumour images featured in Fig. 6A 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 were already under consideration for publication prior to its submission to *International Journal of Molecular Medicine*, the Editor has decided that this paper should be retracted from the Journal. The authors independently contacted the Editorial Office in the light of the concerns raised by the reader, and requested that the paper be retracted from the Journal on account of their failure to preserve the original raw data. The Editor apologizes to the readership for any inconvenience caused. ,