Corrigendum: Targeting ACLY Attenuates Tumor Growth and Acquired Cisplatin Resistance in Ovarian Cancer by Inhibiting the PI3K–AKT Pathway and Activating the AMPK–ROS Pathway
- 1Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, China
- 2Key Laboratory of Gynecology Oncology of Shandong Province, Qilu Hospital of Shandong University, Jinan, China
- 3Shandong Engineering Laboratory for Urogynecology, Qilu Hospital of Shandong University, Jinan, China
- 4Department of Gynecology and Obstetrics, Affiliated Tengzhou Center People’s Hospital of Jining Medical University, Tengzhou, China
By Wei X, Shi J, Lin Q, Ma X, Pang Y, Mao H, Li R, Lu W, Wang Y and Liu P (2021). Front. Oncol. 11:642229. doi: 10.3389/fonc.2021.642229
In the original article, there was a mistake in Figure 5B as published. We recognized by ourself that the picture of “PI3K” was the same as that of “pan-AKT”, we made a mistake when we dragged the original figure into the AI software.
The corrected Figure 5B appears below.
Figure 5 ACLY knockdown inhibited PI3K/AKT pathway and activated AMPK pathway. (A) Western blotting was used to detect the differential expression of ACLY, PI3K/AKT pathway and p-AMPK-a in A2780 and A2780/CDDP cells. (B) Western blotting on A2780/CDDP-NC and A2780/CDDP-shACLY cells, and them under 20μM cisplatin treatment for 48 h, the bands were quantified and analyzed. The bands were quantitated with Image J software, statistical analysis was performed using Student’s t-test. (C) ROS production of the aforementioned cells and them under treatment of 20μM cisplatin for 48 h, statistical analysis was performed using Student’s t-test. (D) Tumor xenograft formation of A2780/CDDP-NC and A2780/CDDP-shACLY cells with treatment of cisplatin, with each group containing five mice. The difference in tumor weights was compared using Student’s t-test. (E) Proliferation of A2780/CDDP cells in respond to different concentration (low-dose, 10–30μM) of SB-204990, the growth curves were analyzed using one-way ANOVA test. (F) 24, 48, and 72 h IC50 of A2780/CDDP cells under treatment of cisplatin combined with different concentration of SB-204990 (from 0 to 30μM), 24 h IC50 of which were 32.34 (26.71–40.60), 16.75 (15.24–18.43), 11.08 (9.736–12.55), 9.495 (7.759–11.38) μM, respectively; 48 h IC50 of which were 25.37 (23.86–27.00), 12.33 (10.74–14.13), 7.983 (7.487–8.499), 6.979 (6.749–7.215) μM; 72 h IC50 of which were 16.96 (14.89–19.34), 9.727 (9.294–10.18), 7.407 (7.083–7.741), 5.922 (5.601–6.246) μM, respectively. All cell experiments were repeated three times at least. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001 for statistical analysis of the indicated groups.
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way.
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Keywords: ACLY, ovarian cancer, cisplatin resistance, PI3K-AKT pathway, AMPK-ROS pathway
Citation: Wei X, Shi J, Lin Q, Ma X, Pang Y, Mao H, Li R, Lu W, Wang Y and Liu P (2021) Corrigendum: Targeting ACLY Attenuates Tumor Growth and Acquired Cisplatin Resistance in Ovarian Cancer by Inhibiting the PI3K–AKT Pathway and Activating the AMPK–ROS Pathway. Front. Oncol. 11:742374. doi: 10.3389/fonc.2021.742374
Received: 16 July 2021; Accepted: 20 August 2021;
Published: 07 September 2021.
Edited and reviewed by:Haifeng Qiu, Zhengzhou University, China
Copyright © 2021 Wei, Shi, Lin, Ma, Pang, Mao, Li, Lu, Wang and Liu. 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.