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CORRECTION article

Front. Cell Dev. Biol., 15 November 2023
Sec. Cell Adhesion and Migration
Volume 11 - 2023 | https://doi.org/10.3389/fcell.2023.1239836

Corrigendum: miR-766-3p targeting BCL9L suppressed tumorigenesis, epithelial-mesenchymal transition, and metastasis through the β-catenin signaling pathway in osteosarcoma cells

www.frontiersin.orgSheng Zhang1 www.frontiersin.orgHongtao Chen1 www.frontiersin.orgWanshun Liu1 www.frontiersin.orgLe Fang2 www.frontiersin.orgZhanyang Qian3 www.frontiersin.orgRenyi Kong1 www.frontiersin.orgQi Zhang4 www.frontiersin.orgJuming Li1* www.frontiersin.orgXiaojian Cao1*
  • 1Department of Orthopedics, First Affiliated Hospital of Nanjing Medical University, Nanjing, China
  • 2Department of Respiratory and Critical Care Medicine, First Affiliated Hospital of Nanjing Medical University, Nanjing, China
  • 3Department of Orthopedics, The Affiliated Zhongda Hospital of Southeast University, Nanjing, China
  • 4Department of Pain Management, Sir Run Run Hospital, Nanjing Medical University, Nanjing, China

A Corrigendum on
miR-766-3p targeting BCL9L suppressed tumorigenesis, epithelial-mesenchymal transition, and metastasis through the β-catenin signaling pathway in osteosarcoma cells

by Zhang S, Chen H, Liu W, Fang L, Qian Z, Kong R, Zhang Q, Li J and Cao X (2020). Front. Cell Dev. Biol. 8:594135. doi: 10.3389/fcell.2020.594135

In the published article, there was an error in Figure 2 as published. The photograph of U2OS N-cadherin WB strip in Figure 2B, the 143B miR-766-3p sh#2 cell migration and invasion photograph of Figures 2E, G are wrong. The corrected Figure 2 and its caption appear below.

FIGURE 2
www.frontiersin.org

FIGURE 2. Downregulating miR-766-3p promoted OS cell EMT, migration and invasion in vitro. (A) miR-766-3p lentiviruses were successfully transfected into 143B and U2OS cell lines (n = 3). (B) miR-766-3p sh#1 and miR-766-3p sh#2 increased the expression level of metastasis-related proteins in 143B and U2OS (n = 3). (C–F) The knockdown of miR-766-3p notably promoted the invasion and migration of 143B and U2OS cells (n = 4). (G, H) The Transwell invasion assays indicated that the knockdown of miR-766-3p significantly increased the invasive ability of OS cells (n = 4). (I–K) Colony formation, CCK-8 and EdU assays demonstrated that downregulating miR-766-3p promoted the proliferation of OS cells (n = 4). Data are presented as the means ± SD. *p < 0.01.

The authors apologize for these errors and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Keywords: osteosarcoma, miR-766-3p, BCL9L, β-catenin, EMT, metastasis

Citation: Zhang S, Chen H, Liu W, Fang L, Qian Z, Kong R, Zhang Q, Li J and Cao X (2023) Corrigendum: miR-766-3p targeting BCL9L suppressed tumorigenesis, epithelial-mesenchymal transition, and metastasis through the β-catenin signaling pathway in osteosarcoma cells. Front. Cell Dev. Biol. 11:1239836. doi: 10.3389/fcell.2023.1239836

Received: 14 June 2023; Accepted: 27 October 2023;
Published: 15 November 2023.

Edited and reviewed by:

Maurizio Onisto, University of Padua, Italy

Copyright © 2023 Zhang, Chen, Liu, Fang, Qian, Kong, Zhang, Li and Cao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Juming Li, lijuming@jsph.org.cn; Xiaojian Cao, xiaojiancao001@163.com

These authors have contributed equally to this work

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