Advertisement

Correction to: EBV-miR-BART8-3p induces epithelial-mesenchymal transition and promotes metastasis of nasopharyngeal carcinoma cells through activating NF-κB and Erk1/2 pathways

  • Cheng Lin
  • Jingfeng Zong
  • Wansong Lin
  • Minghui Wang
  • Yuanji Xu
  • Rui Zhou
  • Shaojun Lin
  • Qiaojuan Guo
  • Honglin Chen
  • Yunbin Ye
  • Bin ZhangEmail author
  • Jianji PanEmail author
Open Access
Correction

Correction to: Journal of Experimental & Clinical Cancer Research (2018) 37:283.

Doi 10.1186/s13046-018-0953-6

Following publication of the original article [1], the authors reported two errors in the article.
  • In the caption of Fig. 1c the sentence “The 20 most highly upregulated EBV BART miRNAs identified between NPC specimens and normal nasopharyngeal mucosal specimens” should instead read “The highly upregulated EBV BART miRNAs identified between NPC specimens and normal nasopharyngeal mucosal specimens”.

  • In Fig. 3a, the first image in the BART8-3p group was inadvertently imported and replaced with the original one in the NC group. A corrected version of Fig. 3 is shown in this Correction.

Fig. 3

Overexpression of EBV-miR-BART8-3p promotes lung metastasis of NPC in vivo. a Nude mice were intravenously injected with SUNE-1-BART8-3p cells or control vector-transfected SUNE-1 cells via the tail veins, and were sacrificed 6 weeks post-injection. Representative images in vivo were obtained by the whole-body imaging system. b Representative images of metastatic nodules in mouse lungs. c Number of metastatic nodules in mouse lungs. d Weight of mouse lungs. *P < 0.05

Reference

  1. 1.
    Lin, et al. EBV-miR-BART8-3p induces epithelial-mesenchymal transition and promotes metastasis of nasopharyngeal carcinoma cells through activating NF-κB and Erk1/2 pathways. J Exp Clin Cancer Res. 2018;37(283).  https://doi.org/10.1186/s13046-018-0953-6.

Copyright information

© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors and Affiliations

  • Cheng Lin
    • 1
    • 2
  • Jingfeng Zong
    • 2
  • Wansong Lin
    • 3
  • Minghui Wang
    • 4
  • Yuanji Xu
    • 2
  • Rui Zhou
    • 1
  • Shaojun Lin
    • 2
  • Qiaojuan Guo
    • 2
  • Honglin Chen
    • 5
  • Yunbin Ye
    • 3
    • 6
  • Bin Zhang
    • 4
    Email author
  • Jianji Pan
    • 2
    Email author
  1. 1.Fujian Medical UniversityFuzhouChina
  2. 2.Department of Radiation OncologyFujian Cancer Hospital & Fujian Medical University Cancer HospitalFuzhouChina
  3. 3.Laboratory of Immuno-OncologyFujian Cancer Hospital & Fujian Medical University Cancer HospitalFuzhouChina
  4. 4.Department of Genetics and Genomic SciencesIcahn Institute of Genomics and Multiscale Biology, Mount Sinai Center for Transformative Disease Modeling, Icahn School of Medicine at Mount SinaiNew YorkUSA
  5. 5.State Key Laboratory for Emerging Infectious Diseases, Department of Microbiology and the Collaborative Innovation Center for Diagnosis and Treatment of Infectious DiseasesThe University of Hong KongHong KongChina
  6. 6.Fujian Provincial Key Laboratory of Translational Cancer MedicineFuzhouChina

Personalised recommendations