Yu J, Xu BT, Li Q, Shang ZT. Tankyrase 2 as a therapeutic target in non-small cell lung cancer: Implications for apoptosis and migration. World J Clin Oncol 2025; 16(3): 103234 [DOI: 10.5306/wjco.v16.i3.103234]
Corresponding Author of This Article
Bo-Tao Xu, MD, Assistant Professor, Postdoctoral Fellow, Department of Cardiothoracic Surgery, Zhuji People’s Hospital, No. 9 Jianmin Road, Taozhu Street, Zhuji 311800, Zhejiang Province, China. 18888755957@163.com
Research Domain of This Article
Respiratory System
Article-Type of This Article
Letter to the Editor
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
World J Clin Oncol. Mar 24, 2025; 16(3): 103234 Published online Mar 24, 2025. doi: 10.5306/wjco.v16.i3.103234
Tankyrase 2 as a therapeutic target in non-small cell lung cancer: Implications for apoptosis and migration
Jing Yu, Bo-Tao Xu, Qiu Li, Zhong-Tu Shang
Jing Yu, Qiu Li, Zhong-Tu Shang, Department of Respiratory Medicine, Zhuji people’s Hospital, Zhuji 311800, Zhejiang Province, China
Bo-Tao Xu, Department of Cardiothoracic Surgery, Zhuji People’s Hospital, Zhuji 311800, Zhejiang Province, China
Author contributions: Yu J and Li Q conceptualization and writing of the original draft; Shang ZT formal analysis and validation; Xu BT conceptualization, writing, reviewing and editing. All authors participated in drafting the manuscript and all have read, contributed to, and approved the final version of the manuscript.
Conflict-of-interest statement: No author has stated that there are any commercial, professional, or personal conflicts of interest relevant to the study, proving that it complies with the principles of publishing ethics.
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: Bo-Tao Xu, MD, Assistant Professor, Postdoctoral Fellow, Department of Cardiothoracic Surgery, Zhuji People’s Hospital, No. 9 Jianmin Road, Taozhu Street, Zhuji 311800, Zhejiang Province, China. 18888755957@163.com
Received: November 13, 2024 Revised: December 14, 2024 Accepted: December 20, 2024 Published online: March 24, 2025 Processing time: 70 Days and 1.9 Hours
Abstract
This letter addresses Wang and Zhang's investigation into the role of tankyrase 2 (TNKS2) as a pivotal driver of malignancy in non-small cell lung cancer (NSCLC) through mechanisms including apoptosis inhibition, enhanced cellular migration, and β-catenin pathway activation. Their study in NSCLC cell lines demonstrates that TNKS2 overexpression stabilizes β-catenin, subsequently triggering oncogenic gene expression and facilitating cellular migration-key attributes of metastatic potential. These insights position TNKS2 as a compelling target for therapy and a potential prognostic marker in NSCLC. Nevertheless, translating these in vitro findings to clinical practice requires validation in in vivo models. Additionally, further research should investigate TNKS2 expression in patient samples and assess its implications in therapy resistance and combination treatment strategies.
Core Tip: Tankyrase 2 (TNKS2) drives the progression of non-small cell lung cancer (NSCLC) by inhibiting apoptosis and promoting cell migration, significantly activating the β-catenin pathway. This function underscores TNKS2's potential as a therapeutic target in NSCLC; however, additional in vivo studies are needed to confirm its role and to evaluate its expression in clinical samples for prognostic use. Combining TNKS2 inhibitors with apoptosis-inducing drugs may enhance therapeutic efficacy, while targeted delivery methods could reduce off-target effects in healthy tissues, advancing the development of TNKS2-focused treatment strategies in NSCLC management.
