This article is a correction to:
Sestrin2-Mediated Autophagy Contributes to Drug Resistance via Endoplasmic Reticulum Stress in Human Osteosarcoma
Zhen Tang1†
Xinghui Wei1†
Tian Li2†Wei Wang3†Hao Wu1Hui Dong1Yichao Liu1Feilong Wei4Lei Shi1Xiaokang Li4*
Zheng Guo4*
Xin Xiao1*- 1Department of Orthopaedics, Xijing Hospital, Fourth Military Medical University, Xi’an, China
- 2School of Basic Medicine, Fourth Military Medical University, Xi’an, China
- 3State Key Laboratory of Cancer Biology, Department of Immunology, Fourth Military Medical University, Xi’an, China
- 4Department of Orthopaedics, Tangdu Hospital, Fourth Military Medical University, Xi’an, China
A Corrigendum on
Sestrin2-mediated autophagy contributes to drug resistance via endoplasmic reticulum stress in human osteosarcoma
by Tang Z, Wei X, Li T, Wang W, Wu H, Dong H, Liu Y, Wei F, Shi L, Li X, Guo Z and Xiao X (2021). Front. Cell Dev. Biol. 9:722960. doi: 10.3389/fcell.2021.722960
In the original article, there was a mistake in Figures 3D,E, 4E as published. The transmission electron microscopy shown in Figures 3D, 4E, and immunofluorescence in Figure 3E were mistakenly used.
FIGURE 3
FIGURE 3. Knockdown of SESN2 resulted in inhibited autophagy and increased apoptosis of osteosarcoma cells treated with chemotherapy. After treatment with Cis (20 μmol/L), Dox (0.2 μg/ml), or Mtx (50 μmol/L) for 24 h, SESN2-knockdown and control cells were subjected to western blot to detect the expression of cleaved and total PARP, LC3, and P62 expression levels (A) (n = 3). SESN2-knockdown HOS cells were treated with Cis (20 μmol/L) for 24 h with or without rapamycin (100 nmol/L) for 6 h. Proliferation was analysed by CCK-8 assay (B) (n = 3), apoptosis was assessed by Annexin V-PE/PI staining (C) (n = 3), and LC3 puncta formation was analysed by immunofluorescence (E) (n = 3, scale bar = 20 µm). Intracellular autophagosomes were observed by TEM (D) (n = 3, scale bar = 2 µm), and autophagic flux was monitored by fluorescence microscopy in HOS cells with transient expression of GFP-RFP-LC3 in HOS cells (F) (n = 3, scale bar = 10 µm). The data are presented as the mean ± SD. *p < 0.05 vs. the Control shRNA group.
FIGURE 4
FIGURE 4. SESN2 regulates autophagy and reduces the sensitivity of osteosarcoma cells to chemotherapy. In the presence or absence of 3-MA (5 mM), SESN2-overexpressing and control HOS cells were treated with Dox (0.2 μg/ml) for 24 h, and apoptosis was analysed by flow cytometry (A) (n = 3). After treatment with Cis (20 μmol/L) or Dox (0.2 μg/ml), the expression levels of LC3 and P62 in SESN2-overexpressing and control HOS cells were detected by western blot (B) (n = 3). The expression levels of LC3 and P62 in SESN2-overexpressing and control HOS cells treated with 3-MA (5 mM) were detected by western blot (C) (n = 3). In the presence or absence of 3-MA (5 mM), SESN2-overexpressing and control HOS cells were treated with Dox (0.2 μg/ml) for 24 h, cell activity was detected by CCK-8 (D) (n = 3), intracellular autophagosomes were observed by TEM (E) (n = 3, scale bar = 2 µm), and intracellular LC3 puncta formation was analysed by immunofluorescence (F) (n = 3, scale bar = 20 µm). After treatment with Cis (20 μmol/L) or Dox (0.2 μg/ml), autophagosome formation in HOS cells with ectopic SESN2 expression was monitored by immunofluorescence through transfection with RFP-GFP-LC3 lentivirus after upregulating SESN2 (G) (n = 3, scale bar = 10 µm). The data are presented as the mean ± SD. *p < 0.05 vs. the pHBLV control group.
The red arrows in the figure legends of Figures 3, 4 are autophagosomes.
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
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Keywords: Sestrin2, apoptosis, autophagy, drug resistance, endoplasmic reticulum stress
Citation: Tang Z, Wei X, Li T, Wang W, Wu H, Dong H, Liu Y, Wei F, Shi L, Li X, Guo Z and Xiao X (2022) Corrigendum: Sestrin2-mediated autophagy contributes to drug resistance via endoplasmic reticulum stress in human osteosarcoma. Front. Cell Dev. Biol. 10:882270. doi: 10.3389/fcell.2022.882270
Received: 23 February 2022; Accepted: 05 September 2022;
Published: 11 October 2022.
Edited and reviewed by:
Andrea Del Fattore, Bambino Gesù Children’s Hospital (IRCCS), ItalyCopyright © 2022 Tang, Wei, Li, Wang, Wu, Dong, Liu, Wei, Shi, Li, Guo and Xiao. 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: Xiaokang Li, lxkfmmu@163.com; Zheng Guo, guozheng@fmmu.edu.cn; Xin Xiao, xiao_xxtyfsxx@sina.com
†These authors have contributed equally to this work