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Results show CNPY3 upregulation associates with advanced stage and worse prognosis, promotes proliferation and migration, and suppresses apoptosis, while also reshaping fibroblast behavior and limiting tumor growth in xenografts.",{"@graph":14,"@context":65},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/healthcare/","Healthcare",3,{"item":32,"name":10,"@type":21,"position":33},"https://docshare.wps.com/document/cnpy3s-regulation-of-tumor-microenvironment-and-its-impact-on-colon-cancer-aggressiveness/364677/",4,{"url":32,"name":10,"@type":35,"image":36,"author":41,"headline":10,"publisher":44,"fileFormat":47,"inLanguage":8,"description":12,"dateModified":48,"datePublished":49,"encodingFormat":47,"isAccessibleForFree":50,"interactionStatistic":51},"DigitalDocument",{"url":37,"@type":38,"width":39,"height":40},"https://docshare.wps.com/thumbnails/cnpy3s-regulation-of-tumor-microenvironment-and-its-impact-on-colon-cancer-aggressiveness/364677.png","ImageObject",300,407,{"name":42,"@type":43},"Asher","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-11-01","2026-09-23",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",13,{"@type":57,"mainEntity":58},"FAQPage",[59],{"name":60,"@type":61,"acceptedAnswer":62},"What do the findings suggest about CNPY3 as a therapeutic target?","Question",{"text":63,"@type":64},"CNPY3 knockdown inhibited key malignant behaviors, altered fibroblast transformation, reduced activation of MAPK and PI3K/AKT pathways, and increased sensitivity to 5-fluorouracil. 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Molecular Medicine (2025) 31:89 Molecular Medicine  \n[https://doi.org/10.1186/s10020-025-01145-1](https://doi.org/10.1186/s10020-025-01145-1)  \nRESEARCH Open Access  \nCNPY3’s regulation of tumor microenvironment and its impact on colon cancer aggressiveness  \nXucan Gao 1*, Biaohuan Zhou 1, Xiudong Feng2, Zhouxin Ji 1, Qiang Li 1 and Huining Liu 1  \nAbstract  \nBackground Canopy FGF signaling regulator 3 (CNPY3) has been implicated in tumor progression. However, its specific role in colon cancer (CC) remains unclear. This study aims to investigate the function of CNPY3 in CC and its potential as a therapeutic target.  \nMethods A total of 201 CC tissue specimens and 67 adjacent non-cancerous tissues were collected for analysis. CNPY3 expression was assessed using immunohistochemistry and quantitative real-time PCR. Functional assays were conducted in CC cell lines (HT-29 and SW-620) following CNPY3 knockdown to evaluate its effects on cell proliferation, migration, and apoptosis. Gene expression profiling, fibroblast co-culture experiments, and in vivo xenograft models were also conducted.  \nResults Increased CNPY3 expression correlated with advanced tumor stages and poorer prognosis. Knockdown of CNPY3 significantly inhibited cell proliferation, migration, and induced apoptosis in CC cell lines. CNPY3 depletion also modulated fibroblast behavior, inhibiting their transformation into cancer-associated fibroblasts. Pathway analysis revealed that CNPY3 knockdown affected the cell cycle and p53 signaling pathways, and reduced activation of the MAPK and PI3K/AKT pathways. Additionally, CNPY3 knockdown enhanced CC cell sensitivity to 5-fluorouracil. In vivo studies demonstrated that CNPY3 knockdown resulted in smaller tumor sizes and weights than controls.  \nConclusions CNPY3 is a crucial regulator in CC progression, correlating with tumor aggressiveness and poor patient outcomes. Targeting CNPY3 may offer a promising therapeutic strategy and a valuable prognostic marker in CC management.  \nKeywords CNPY3, Colon cancer, Tumor microenvironment, Biomarker, Tumorigenesis  \n*Correspondence: Xucan Gao [logia@szhospital.com](logia@szhospital.com)  \n1Department of Anorectal Surgery, Shenzhen People’s Hospital (The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen, Guangdong 518020, China  \n2Department of Operating Room, Shenzhen People’s Hospital (The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen, Guangdong 518020, China  \n© The Author(s) 2025. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit [http://creativecommons.org/l](http://creativecommons.org/l)icenses/by/4.0/.  \nGao et al. Molecular Medicine (2025) 31:89  \nBackground  \nColon cancer (CC) is one of the leading causes of cancerrelated mortality worldwide, marked by high recurrence and metastasis rates that complicate treatment efforts (Benson et al. 2024). The global burden of CC is substantial. It ranks as the third most commonly diagnosed cancer and the second leading cause of cancer death, according to World Health Organization statistics (Chalabi et a","cbCaid7MtwWk4aj3","https://ap.wps.com/l/cbCaid7MtwWk4aj3","pdf",17854936,15,"English","# Background\n## Colon cancer burden and unmet clinical needs\n## Tumor microenvironment and cancer-associated fibroblasts (CAFs)\n## Prior pathway findings and rationale for CNPY3\n# Methods\n## Patient tissue collection\n## Expression assessment\n## Cell functional assays after knockdown\n## Co-culture and xenograft experiments\n# Results\n## Clinical correlation with tumor stage and prognosis\n## Effects on proliferation, migration, and apoptosis\n## Impact on fibroblast transformation\n## Pathway changes and drug sensitivity\n## In vivo tumor suppression\n# Conclusions\n## Therapeutic targeting and prognostic value","[{\"question\":\"What do the findings suggest about CNPY3 as a therapeutic target?\",\"answer\":\"CNPY3 knockdown inhibited key malignant behaviors, altered fibroblast transformation, reduced activation of MAPK and PI3K/AKT pathways, and increased sensitivity to 5-fluorouracil. Xenograft experiments showed smaller tumor sizes and weights after CNPY3 depletion.\"}]","CNPY3’s regulation of tumor microenvironment and its impact on colon cancer aggressiveness | PDF",1790158718,38]