Li BC, Wang BZ, Han L, Zhang ZW, Wang Y, Zhang YJ, Zhang JN. Goosecoid drives colorectal cancer progression by inducing epithelial-mesenchymal transition. World J Gastrointest Oncol 2026; 18(3): 115028 [DOI: 10.4251/wjgo.v18.i3.115028]
Corresponding Author of This Article
Jiu-Na Zhang, PhD, Department of Gastroenterology, The Affiliated Hospital of Hebei University of Engineering, No. 81 Congtai Road, Handan 056002, Hebei Province, China. zhangjiuna@hebeu.edu.cn
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Basic Study
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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/
Mar 15, 2026 (publication date) through Mar 12, 2026
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Journal Information of This Article
Publication Name
World Journal of Gastrointestinal Oncology
ISSN
1948-5204
Publisher of This Article
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
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Li BC, Wang BZ, Han L, Zhang ZW, Wang Y, Zhang YJ, Zhang JN. Goosecoid drives colorectal cancer progression by inducing epithelial-mesenchymal transition. World J Gastrointest Oncol 2026; 18(3): 115028 [DOI: 10.4251/wjgo.v18.i3.115028]
Bai-Chao Li, Bing-Zhe Wang, Liang Han, School of Clinical Medicine, Hebei University of Engineering, Handan 056002, Hebei Province, China
Zhi-Wei Zhang, Department of Oncology, The Affiliated Hospital of Hebei University of Engineering, Handan 056002, Hebei Province, China
Ying Wang, Department of Geriatrics, The Affiliated Hospital of Hebei University of Engineering, Handan 056002, Hebei Province, China
Yong-Jian Zhang, Jiu-Na Zhang, Department of Gastroenterology, The Affiliated Hospital of Hebei University of Engineering, Handan 056002, Hebei Province, China
Co-first authors: Bai-Chao Li and Bing-Zhe Wang.
Author contributions: Li BC and Wang BZ collected the data and wrote the manuscript as co-first authors; Han L and Zhang ZW participated in the discussion; Wang Y and Zhang YJ arranged the experimental data; Zhang JN reviewed the manuscript and provided funding support; all authors read and approved the final manuscript.
Supported by Natural Science Foundation of Hebei Province (General Program), No. H2022402009; Precision Medicine Joint Cultivation Fund Project of Hebei Natural Science Foundation, No. H2021402007; Hebei Provincial Department of Finance, No. ZF2023221; and Cooperative Project of the Affiliated Hospital of Hebei University of Engineering, No. KFKT2024-05.
Institutional review board statement: The study was reviewed and approved by the Ethics Committee of the Affiliated Hospital of Hebei University of Engineering, No. 2021[K]112.
Conflict-of-interest statement: All authors declare no conflict of interest in publishing the manuscript.
Data sharing statement: There is no conflict of interest in this study.
Corresponding author: Jiu-Na Zhang, PhD, Department of Gastroenterology, The Affiliated Hospital of Hebei University of Engineering, No. 81 Congtai Road, Handan 056002, Hebei Province, China. zhangjiuna@hebeu.edu.cn
Received: October 11, 2025 Revised: November 24, 2025 Accepted: January 14, 2026 Published online: March 15, 2026 Processing time: 157 Days and 17.3 Hours
Abstract
BACKGROUND
Colorectal cancer (CRC) poses a substantial public health burden worldwide, consistently exhibiting a notable incidence among malignancies across the globe. Goosecoid (GSC), an evolutionarily conserved homeodomain transcription factor, is recognized as a pivotal organizer gene during embryonic development and has been increasingly associated with oncogenic processes. Despite its established roles in other cancers, the specific functions and molecular mechanisms of GSC in the pathogenesis of CRC remain to be fully elucidated. This study therefore aimed to investigate the contribution of GSC to CRC progression and elucidate the underlying mechanistic pathways.
AIM
To investigate the oncogenic properties of GSC and elucidate its mechanism of action in CRC.
METHODS
We validated the expression levels of GSC in CRC tissues using the UALCAN database, Western blotting, immunohistochemistry, and immunofluorescence. The association between GSC and CRC prognosis was analyzed via the Kaplan-Meier Plotter database. The effects of GSC on CRC proliferation, invasion, and metastasis were systematically evaluated through a set of functional assays, such as colony formation assay, Transwell migration and invasion assay, wound healing assay, and tube formation assay.
RESULTS
Through the UALCAN database, Kaplan-Meier Plotter database, western blotting, immunohistochemistry, and immunofluorescence, we found that GSC was significantly upregulated in CRC. High expression of GSC in CRC was associated with poorer recurrence-free survival and overall survival. Furthermore, in vitro studies showed that knocking down GSC inhibited the epithelial-mesenchymal transition (EMT) process, proliferation, invasion, and metastasis of CRC cells; conversely, overexpression of GSC significantly enhanced the EMT process, proliferation, invasion, and metastasis of CRC cells. Mechanistically, we found that knockdown and overexpression of GSC altered the abundance of target proteins linked to the Wnt/β-catenin signaling cascade.
CONCLUSION
By activating the Wnt/β-catenin signaling axis, GSC drives CRC progression and EMT, positioning it as a viable diagnostic and therapeutic target.
Core Tip: Goosecoid (GSC) is significantly upregulated in colorectal cancer (CRC) tissues and cell lines, with its elevated expression correlated with unfavorable patient outcomes. Functional analyses demonstrate that GSC knockdown attenuates CRC cell proliferation, migration, and invasion. Mechanistically, these inhibitory effects are mediated through the Wnt/β-catenin signaling pathway, concomitant with the regulation of key epithelial-mesenchymal transition markers. Collectively, our findings establish GSC as a critical promoter of CRC growth and metastatic dissemination.
