{"title":"B7-H3 enhances the malignant phenotype of colorectal cancer by activating the Wnt/β-catenin pathway mediated by CYP1B1","authors":"Xingxiang Liu , Jie Ding , Qiumei Zong , Yong Mao","doi":"10.1016/j.tice.2025.103066","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Colorectal cancer (CRC) is a prevalent malignancy. Previous studies have identified aberrant expression of Cytochrome P450 1B1 (CYP1B1) in human CRC tissues; however, the exact role and molecular mechanism of CYP1B1 in CRC remain unknown.</div></div><div><h3>Methods</h3><div>This study initially assessed the expression of CYP1B1 in human colorectal cancer samples and cell lines. Subsequently, siRNA or overexpression plasmid of CYP1B1 was transfected into CaCo-2 or SW480 cells, and cell proliferation, cycle, migration, and invasion were analyzed using CCK8, Colony-formation, Ethynyl-20-deoxyuridine incorporation, flow cytometry, wound healing and transwell assays, and the expression level of CYP1B1 was determined by quantitative real-time polymerase chain reaction and western blotting.</div></div><div><h3>Results</h3><div>The results indicated that up-regulation of CYP1B1 in CRC samples compared to normal tissues, with its expression level correlating with the local infiltration status. CYP1B1 influenced the proliferation of CRC cells, induced epithelial-mesenchymal transition through the Wnt/β-catenin pathway, thereby promoting cell migration and invasion. Additionally, CYP1B1 expression could be regulated by B7-H3 through the PI3K-AKT pathway.</div></div><div><h3>Conclusions</h3><div>Those findings suggested that overexpression of CYP1B1 enhances the migration and invasion of human CRC cells by activating the PI3K/Akt signaling pathway through B7-H3.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103066"},"PeriodicalIF":2.5000,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tissue & cell","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0040816625003465","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ANATOMY & MORPHOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background
Colorectal cancer (CRC) is a prevalent malignancy. Previous studies have identified aberrant expression of Cytochrome P450 1B1 (CYP1B1) in human CRC tissues; however, the exact role and molecular mechanism of CYP1B1 in CRC remain unknown.
Methods
This study initially assessed the expression of CYP1B1 in human colorectal cancer samples and cell lines. Subsequently, siRNA or overexpression plasmid of CYP1B1 was transfected into CaCo-2 or SW480 cells, and cell proliferation, cycle, migration, and invasion were analyzed using CCK8, Colony-formation, Ethynyl-20-deoxyuridine incorporation, flow cytometry, wound healing and transwell assays, and the expression level of CYP1B1 was determined by quantitative real-time polymerase chain reaction and western blotting.
Results
The results indicated that up-regulation of CYP1B1 in CRC samples compared to normal tissues, with its expression level correlating with the local infiltration status. CYP1B1 influenced the proliferation of CRC cells, induced epithelial-mesenchymal transition through the Wnt/β-catenin pathway, thereby promoting cell migration and invasion. Additionally, CYP1B1 expression could be regulated by B7-H3 through the PI3K-AKT pathway.
Conclusions
Those findings suggested that overexpression of CYP1B1 enhances the migration and invasion of human CRC cells by activating the PI3K/Akt signaling pathway through B7-H3.
期刊介绍:
Tissue and Cell is devoted to original research on the organization of cells, subcellular and extracellular components at all levels, including the grouping and interrelations of cells in tissues and organs. The journal encourages submission of ultrastructural studies that provide novel insights into structure, function and physiology of cells and tissues, in health and disease. Bioengineering and stem cells studies focused on the description of morphological and/or histological data are also welcomed.
Studies investigating the effect of compounds and/or substances on structure of cells and tissues are generally outside the scope of this journal. For consideration, studies should contain a clear rationale on the use of (a) given substance(s), have a compelling morphological and structural focus and present novel incremental findings from previous literature.