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CORRECTION article

Front. Oncol., 12 January 2026

Sec. Women's Cancer

Volume 15 - 2025 | https://doi.org/10.3389/fonc.2025.1722174

Correction: Chidamide combined with doxorubicin induced p53-driven cell cycle arrest and cell apoptosis reverse multidrug resistance of breast cancer

This article is a correction to:

  1. Chidamide Combined With Doxorubicin Induced p53-Driven Cell Cycle Arrest and Cell Apoptosis Reverse Multidrug Resistance of Breast Cancer

    1. Read original article
Lixia Cao&#x;Lixia Cao†Shaorong Zhao&#x;Shaorong Zhao†Qianxi Yang&#x;Qianxi Yang†Zhendong ShiZhendong ShiJingjing LiuJingjing LiuTeng PanTeng PanDongdong ZhouDongdong ZhouJin Zhang*Jin Zhang*
  • Third Department of Breast Surgery, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Clinical Research Center for Cancer, Tianjin, China

A Correction on
Chidamide combined with doxorubicin induced p53-driven cell cycle arrest and cell apoptosis reverse multidrug resistance of breast cancer

By Cao L, Zhao S, Yang Q, Shi Z, Liu J, Pan T, Zhou D and Zhang J (2021) Front. Oncol. 11:614458. doi: 10.3389/fonc.2021.614458

There was a mistake in “Figure 1 and Figure 2” as published. In “Figure 1E”, the Western blot image for GAPDH was incorrectly uploaded. In “Figure 2B, C”, the mistake was caused by an unintentional assembly mistake. In “Figure 2B”, an inadvertent image duplication occurred between the CON and DOX groups in the CALDOX cell line. In “Figure 2C”, it has come to our attention that the data presented were inadvertently taken from a different experimental replicate. The corrected “Figure 1 and Figure 2” appears below.

Figure 1
Charts and blots demonstrate drug effects on cell survival and protein expression. Panel A and B show cell survival rates with increasing doses of Doxorubicin and Chidamide in CAL51, CALDOX, MCF-7, and MCF-7/A02 cells. Bar graphs indicate IC50 values. Panel C shows combination index plots for CALDOX and MCF-7/A02. Panels D and E display Western blots for HDAC1 and GAPDH under different conditions. Panel F shows acetylation levels of H3K9 and H3K18 in CALDOX and MCF-7/A02 cells treated with DOX and CHI.

Figure 1. Effects of chidamide (CHI) and/or doxorubicin (DOX) on the viability and histone H3 acetylation of MDR breast cancer cells. (A) IC50 values of DOX of two pairs of human breast cancer cell lines and their multidrug-resistant (MDR) sublines. (B) IC50 values of CHI of two pairs of human breast cancer cell lines and their MDR sublines. (C) Cytotoxicity of CHI and DOX to CALDOX and MCF-7/A02 cells. (D) Expression of HDAC1 in sensitive and resistant cell lines. (E) Effects of CHI and DOX on HDAC1 expression in drug-resistant cells. (F) Effects of CHI and DOX on acetylation of H3K9 and H3K18 in drug-resistant cells. H3 was used as a loading control. The numerical values are expressed as mean ± standard deviation (SD) of three independent replicates. *P < 0.05, ***P < 0.001.

Figure 2
Panel A shows a series of cell colony images treated with DOX and CHI, along with a bar graph comparing cell viability between CALDOX and MCF-7/A02 groups. Panel B presents DAPI and EDU stained cells with a bar graph indicating EDU incorporation rates. Panel C includes histograms of cell cycle distribution with propidium iodide staining, displaying different phases, and corresponding bar graphs for CALDOX and MCF-7/A02 groups.

Figure 2. Effects of chidamide (CHI) and/or doxorubicin (DOX) on the proliferation and cell cycle of multidrug-resistant (MDR) breast cancer cells. (A) Drug resistance clonogenic assay confirmed the effect of CHI and/or DOX on cell proliferation. (B) EDU staining confirmed the effect of CHI and/or DOX on cell proliferation. (C) Effects of CHI and/or DOX on cell cycle. Numerical values are expressed as mean ± SD of three independent replicates. “*” indicates a significant difference compared with the control group (*P < 0.05, **P < 0.01), ”#” indicates a significant difference compared with the DOX-treated group (###P<0.001), and “&” indicates a significant difference compared with the CHI-treated group (&P<0.05).

The original version of this 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: breast cancer, histone deacetylase, chidamide, doxorubicin, drug resistance

Citation: Cao L, Zhao S, Yang Q, Shi Z, Liu J, Pan T, Zhou D and Zhang J (2026) Correction: Chidamide combined with doxorubicin induced p53-driven cell cycle arrest and cell apoptosis reverse multidrug resistance of breast cancer. Front. Oncol. 15:1722174. doi: 10.3389/fonc.2025.1722174

Received: 10 October 2025; Accepted: 23 December 2025; Revised: 23 October 2025;
Published: 12 January 2026.

Edited and reviewed by:

Sharon R. Pine, University of Colorado Anschutz Medical Campus, United States

Copyright © 2026 Cao, Zhao, Yang, Shi, Liu, Pan, Zhou and Zhang. 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: Jin Zhang, emhhbmdqaW50am11Y2gxQDE2My5jb20=

†These authors have contributed equally to this work and share first authorship

Disclaimer: 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.