Immune regulation of Chidamide-induced Linc01010 accumulation in breast cancer cell death

doi:10.5306/wjco.v16.i11.112514

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World Journal of Clinical Oncology

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2218-4333

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

Basic Study

World J Clin Oncol. Nov 24, 2025; 16(11): 112514
Published online Nov 24, 2025. doi: 10.5306/wjco.v16.i11.112514

Immune regulation of Chidamide-induced Linc01010 accumulation in breast cancer cell death

Han Han, Xiao-Yun Guo, Jia-Xin Wen, Xiao-Ming Zhao, Wei-Qiang Zhou

Han Han, Department of Biochemistry and Molecular Biology, Shenyang Medical College, Shenyang 110034, Liaoning Province, China

Xiao-Yun Guo, Jia-Xin Wen, Xiao-Ming Zhao, Wei-Qiang Zhou, Department of Pathogen Biology, Shenyang Medical College, Shenyang 110034, Liaoning Province, China

Author contributions: Han H and Zhou WQ participated in the design of the study and analyzed data; Zhou WQ wrote the manuscript; all authors performed the experiments, reviewed and participated in the manuscript revision.

Supported by Natural Science Combination Foundation for Improving Innovation of Liaoning Province, No. 2022-NLTS-14-01.

Institutional review board statement: This study complied with the relevant regulations of the institution and allowed for relevant experiments to be conducted.

Institutional animal care and use committee statement: The animal experiments involved in this study complied with the relevant regulations of the institution and were allowed to be conducted.

Conflict-of-interest statement: The authors declare no conflict of interest, financial or otherwise.

ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.

Data sharing statement: We are willing to share the relevant experimental results with data.

Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/

Corresponding author: Wei-Qiang Zhou, PhD, Dean, Professor, Department of Pathogen Biology, Shenyang Medical College, No. 146 North Huanghe Street, Shenyang 110034, Liaoning Province, China. zhouwq@hotmail.com

Received: July 29, 2025
Revised: August 12, 2025
Accepted: October 13, 2025
Published online: November 24, 2025
Processing time: 115 Days and 1.4 Hours

Abstract

BACKGROUND

Breast cancer is a prevalent malignant tumor among women. Despite significant advancements in the development and implementation of various anti-breast cancer therapies, enhancing the efficacy of these drugs while minimizing their toxicity remains a challenge.

AIM

To explore the functional impact of the targeted long chain non-coding RNA (LncRNA) of Chidamide on the activity of natural killer (NK) cells via programmed death-ligand 1 (PD-L1), particularly focusing on the mechanisms by which NK cells influence breast cancer cells.

METHODS

This study screened the positive LncRNA molecule Linc01010 through high-throughput sequencing, which can counteract the pharmacological effects of Chidamide. Luciferase localization analysis revealed that the Linc01010 fragment was situated in the proximal exon 4-3 region, identified as its functionally active region. Electrophoretic mobility shift assays and RNA-protein pull-down experiments demonstrated the interaction between Chidamide-induced Linc01010 expression and the target protein mitogen-activated protein kinase kinase 6 (MKK6). Western blotting and quantitative polymerase chain reaction analyses indicated that Chidamide enhanced the expression of the downstream effector PD-L1 by activating the corresponding p38-mitogen-activated protein kinases pathway.

RESULTS

While investigating the effects of the Chidamide-Linc01010-MKK6-PD-L1 axis on the immune cell line NK-92, we observed that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) secretion was significantly inhibited by this response axis. Furthermore, reducing TRAIL secretion within the tumor microenvironment diminished the death effects in breast cancer cells induced by Chidamide.

CONCLUSION

Our study provides a robust foundation for improving the effectiveness of current anti-breast cancer medications and for identifying new targets related to drug resistance.

Keywords: Breast cancer; Linc01010; Chidamide; Mitogen-activated protein kinase kinase 6; Programmed death-ligand 1; Natural killer cells

Core Tip: Breast cancer is a prevalent malignant tumor among women. This study screened the positive long chain non-coding RNA molecule Linc01010 which can counteract the pharmacological effects of Chidamide. While investigating the effects of the Chidamide-Linc01010-mitogen-activated protein kinase kinase 6-programmed death-ligand 1 axis on the immune cell line natural killer-92, we observed that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) secretion was significantly inhibited by this response axis. Furthermore, reducing TRAIL secretion within the tumor microenvironment diminished the death effects in breast cancer cells induced by Chidamide. Our study provides a robust foundation for improving the effectiveness of current anti-breast cancer medications and for identifying new targets related to drug resistance.