miR‑647 and miR‑1914 promote cancer progression equivalently by downregulating nuclear factor IX in colorectal cancer
Authors: Dingding Qu
Shaoqing Liu
Weiping Li
Jianyong Zheng
Liangliang Shen
Qingchuan Zhao
Shisen Li
Jian Zhang
Guosheng Wu
Chenxiang He
Journal: Molecular Medicine Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNAs; colorectal cancer; genetic profiles; cell proliferation; migration
Affiliations: Department of Digestive Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China., Department of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China., Department of Neurology, Second Affiliated Hospital, Shaanxi University of Chinese Medicine, Xi'an, Shaanxi 712046, P.R. China.

Abstract:  MicroRNAs (miRNAs/miRs) have been investigated as diagnostic and prognostic biomarkers for cancer; however, the significance of miRNAs in colorectal cancer (CRC) remains to be elucidated. The aim of the present study was to determine the genetic profiles of CRC tissue, and screen for miRNAs implicated in CRC cell proliferation and migration. RNA sequencing of 10 paired specimens was performed to for screen genes that were upregulated or downregulated in CRC. miRNA expression in CRC specimens and cell lines was confirmed using qPCR analysis. The significance of indicated miRNAs in CRC cell proliferation and migration was evaluated using MTT and scratch wound‑healing assays. Online computational prediction, isobaric tags for relative and absolute quantification analysis and a luciferase reporter assay were applied to determine candidate targeted genes for the miRNAs. RNA‑seq data revealed miR‑1914 as the most prominent miRNA in CRC specimens. qPCR analysis also suggested that the expression of miR‑1914, as well as its counterpart miR‑647 were elevated in CRC specimens and cell lines. Suppression of miR‑647/1914 using small interfering RNAs inhibited CRC SW480 and SW620 cell proliferation, and migration. Nuclear factor I/X (NFIX) was demonstrated to be a candidate for miR‑647/1914 and mediated the oncogenic activity of miR‑647/1914. In all, miR‑647 and miR‑1914 were demonstrated to promote the proliferation and migration of CRC cells by directly targeting NFIX. Therapeutic delivery of siRNAs targeting miR‑647/1914 and overexpression of NFIX may be feasible approaches for CRC treatment. 

Retracted: No

PubPeer comments:
 Figure 3A. * Red boxes: Two panels representing different experimental groups appear to overlap ![file] , 
 Dear Professor, We are glad to receive your comment. The two panels you marked in red did use the same image by mistake, we checked our raw data seriously, and had corrected the mistake. We made the corrected Fig and added the raw data we used in the paper in attachment. Thank you for your serious attitude and comments to help us improve. ![file] Yours sincerely. Dr Jianyong Zheng, Department of Digestive Surgery, Xijing Hospital, The Air Force Military Medical University, Xi an, Shaanxi 710032, P.R. China , 
 Corrigendum, [20 April 2022] .  Subsequently to the publication of this paper, an interested reader drew to the authorsu2019 attention that, in the scratchu2011wound assays shown in Fig. 3A on p. 8195, the data shown for the u20180 h NCu2019 and u20180 h miRu20111914 antagomiru2019 data panels appeared to be strikingly similar, such that they may have been derived from the same original source. The authors have consulted their original data, and realize that the u20180 h miRu20111914 antagomiru2019 data panel was inadvertently selected incorrectly for Fig. 3A. The corrected version of Fig. 3, now showing the correct data for the u20180 h miRu20111914 antagomiru2019 data panel in Fig. 3A, is shown on the next page. Note that the errors in Fig. 3 did not significantly affect the results or the conclusions reported in this paper, and all the authors agree to this Corrigendum. The authors are grateful to the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused. ,