ORIGINAL RESEARCH article
Front. Oncol.
Sec. Molecular and Cellular Oncology
This article is part of the Research TopicDNA Damage, Repair and Mutagenesis: Targeting Cancer’s Achilles HeelView all 9 articles
Identification of ZFP161 as a regulator of the c-Myc oncogene in human colon tissue
Provisionally accepted- 1Soonchunhyang University, Asan-si, Republic of Korea
- 2Hunan University College of Biology, Changsha, China
- 3Mayo Clinic Minnesota Department of Oncology, Rochester, United States
- 4Soonchunhyang Institute of Medi-bio Science, Soonchunhyang University, Cheon-an, Republic of Korea
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Zinc Finger Protein 161 (ZFP161) is a key regulator of Ataxia Telangiectasia and Rad3-related (ATR) signaling, playing a crucial role in maintaining genomic stability. ZF5 is a mouse ortholog of ZFP161 that serves as a putative transcriptional repressor of c-Myc. In this study, we identified ZFP161 as a direct regulator of c-Myc. ZFP161 binds to the promoter region of c-Myc, modulating its expression and downstream signaling pathways. Additionally, ZFP161 promotes cell proliferation and tumorigenesis through c-Myc regulation and contributes to the malignant transformation of RPE-1 cells. High ZFP161 expression is associated with poor survival in patients with mixed colon adenocarcinoma. These findings suggest that ZFP161 plays a role in c-Myc regulation and may represent a potential therapeutic target in c-Myc-driven cancers.
Keywords: c-Myc, c-Myc downstream pathway, tumor development, ZFP161, Zinc finger protein
Received: 06 Aug 2025; Accepted: 11 Dec 2025.
Copyright: © 2025 Christyani, Zhao, Feng, Lee, TU, Zhang, Lou and Kim. 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) or licensor 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: Wootae Kim
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