This article is a correction to:
CDKL3 Targets ATG5 to Promote Carcinogenesis of Esophageal Squamous Cell Carcinoma
Suna Zhou
Mingxin Zhang
Chao Zhou1,2- 1Laboratory of Cellular and Molecular Radiation Oncology, The Affiliated Taizhou Hospital, Wenzhou Medical University, Taizhou, China
- 2Department of Radiation Oncology, The Affiliated Taizhou Hospital, Wenzhou Medical University, Taizhou, China
- 3Department of Gastroenterology, The First Affiliated Hospital of Xi’an Medical University, Xi’an, China
- 4Department of Gastroenterology, The Affiliated Taizhou Hospital, Wenzhou Medical University, Taizhou, China
A Corrigendum on
CDKL3 Targets ATG5 to Promote Carcinogenesis of Esophageal Squamous Cell Carcinoma
By Zhou S, Zhang M, Zhou C, Wang W, Yang H and Ye W (2020). Front. Oncol. 10:1602. doi: 10.3389/fonc.2020.01602
In the original article, there was an error in the Methods section of the Abstract. We carelessly wrote FLVCR1 instead of CDKL3.
A correction has been made to the Methods section of the Abstract, paragraph 2:
“Methods: ESCC samples were stained by immunohistochemical staining (IHC) and analyzed for the expression of CDKL3. The functions of CDKL3 on proliferation, apoptosis, migration, invasion, and colony formation were investigated by celigo assay, MTT assay, colony formation, caspase 3/7 activity analysis, transwell migration and invasion assay, respectively. A transplanted tumor model was established to study the functions of CDKL3 on the tumorigenesis of ESCC cells. Microarray analysis was utilized to identify the CDKL3-regulated genes in ESCC cells.”
In the original article, there was a mistake in the legend for FIGURE 5(F) as published. “genes” was erroneously written as “CSE1L/RPS15A/SFPQ/CAPZB”. The correct legend appears below.
“Figure 5. ATG5 is a potential target of CDKL3. (A) A scatter plot demonstrated the distribution of the signal intensity between two groups in a Cartesian coordinate plane. The X-axis represents KYSE-150-shCtrl group, and the Y-axis represents the KYSE-150-shCDKL3 group. The dots above the upper parallel line represented the downregulated genes, while the dots under the lower parallel line represented the upregulated genes. (B) Volcano Plot exhibited the significantly differentially expressed genes between the two groups. The X-axis denotes the log2-fold difference and the Y-axis denotes the log10-corrected significant. The red dots represented the differentially expressed genes screened with the absolute value of Fold Change ≥1.5 and FDR < 0.05. (C) The interaction network illustrated the interrelationships among these 22 selected genes surrounding the regulation of CDKL3. The up-regulation gene was red while the down-regulation gene was green. The solid line represented the direct interactions while the broken lines represented the indirect interactions, and an arrow represented the activation. (D) RT-PCR was used to confirm the up-regulated and down-regulated genes induced by CDKL3 knockdown in KYSE-150 cells. (E) The expression patterns of the potential interacting genes in the TCGA database according to tumor histology. (F) Comparison of overall survival of esophageal cancer patients with different genes expression based on TCGA data. Data were represented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001 vs. controls, respectively.”
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.
Keywords: cyclin-dependent kinase-like 3, autophagy-related gene 5, esophageal squamous cell carcinoma, prognosis, carcinogenesis
Citation: Zhou S, Zhang M, Zhou C, Wang W, Yang H and Ye W (2021) Corrigendum: CDKL3 Targets ATG5 to Promote Carcinogenesis of Esophageal Squamous Cell Carcinoma. Front. Oncol. 10:619438. doi: 10.3389/fonc.2020.619438
Received: 20 October 2020; Accepted: 24 December 2020;
Published: 04 March 2021.
Edited and reviewed by: Alfredo Criollo, University of Chile, Chile
Copyright © 2021 Zhou, Zhang, Zhou, Wang, Yang and Ye. 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: Haihua Yang, yanghh@enzemed.com; Wenguang Ye, yewenguang_1982@163.com
†These authors have contributed equally to this work