{"title":"FNDC1 Facilitates Proliferation, Migration, and Invasion of Breast Cancer Cells Through Modulating Wnt/β-Catenin Pathway.","authors":"Guocai Fan, Chen Zhang","doi":"10.1007/s10528-024-10994-0","DOIUrl":null,"url":null,"abstract":"<p><p>Breast cancer is the most common malignant cancer and the leading fatal cancer in women around the world. Fibronectin type III domain-containing protein 1 (FNDC1) has been demonstrated to play crucial roles in various tumors. However, the function of FNDC1 in breast cancer remains to be addressed. Increased FNDC1 expression was found in breast cancer that is associated with individual cancer stages and lymph node metastasis through UALCAN analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assays indicated that FNDC1 expression was up-regulated in breast cancer cells. The results of Cell Counting Kit-8 and colony formation assays indicated that FNDC1 promoted the proliferation of breast cancer cells. Moreover, FNDC1 knockdown suppressed xenograft tumor growth and inhibited the levels of FNDC1 and marker of proliferation Ki-67. Transwell assay demonstrated that FNDC1 promoted the migration and invasion of breast cancer cells. Importantly, mechanism analysis implied that FNDC1 promoted the Wnt/β-catenin signaling pathway. Notably, Wnt/β-catenin activation with LiCl significantly enhanced the proliferation and epithelial-mesenchymal transformation (EMT) inhibition effect of silencing FNDC1, whereas Wnt/β-catenin inhibition with XAV-939 significantly weakened the proliferation and EMT promotion effect of FNDC1. Analysis of β-catenin expression in the nucleus and cytoplasm showed that FNDC1 promoted β-catenin nuclear translocation. These data suggested that FNDC1 exerts its oncogene function through modulating Wnt/β-catenin signaling pathway. In conclusion, FNDC1 promotes cell proliferation, migration, invasion, and EMT through modulating Wnt/β-catenin signaling pathway in breast cancer, providing a new idea for the development of breast cancer therapeutic targets.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1000,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochemical Genetics","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s10528-024-10994-0","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Breast cancer is the most common malignant cancer and the leading fatal cancer in women around the world. Fibronectin type III domain-containing protein 1 (FNDC1) has been demonstrated to play crucial roles in various tumors. However, the function of FNDC1 in breast cancer remains to be addressed. Increased FNDC1 expression was found in breast cancer that is associated with individual cancer stages and lymph node metastasis through UALCAN analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assays indicated that FNDC1 expression was up-regulated in breast cancer cells. The results of Cell Counting Kit-8 and colony formation assays indicated that FNDC1 promoted the proliferation of breast cancer cells. Moreover, FNDC1 knockdown suppressed xenograft tumor growth and inhibited the levels of FNDC1 and marker of proliferation Ki-67. Transwell assay demonstrated that FNDC1 promoted the migration and invasion of breast cancer cells. Importantly, mechanism analysis implied that FNDC1 promoted the Wnt/β-catenin signaling pathway. Notably, Wnt/β-catenin activation with LiCl significantly enhanced the proliferation and epithelial-mesenchymal transformation (EMT) inhibition effect of silencing FNDC1, whereas Wnt/β-catenin inhibition with XAV-939 significantly weakened the proliferation and EMT promotion effect of FNDC1. Analysis of β-catenin expression in the nucleus and cytoplasm showed that FNDC1 promoted β-catenin nuclear translocation. These data suggested that FNDC1 exerts its oncogene function through modulating Wnt/β-catenin signaling pathway. In conclusion, FNDC1 promotes cell proliferation, migration, invasion, and EMT through modulating Wnt/β-catenin signaling pathway in breast cancer, providing a new idea for the development of breast cancer therapeutic targets.
期刊介绍：
Biochemical Genetics welcomes original manuscripts that address and test clear scientific hypotheses, are directed to a broad scientific audience, and clearly contribute to the advancement of the field through the use of sound sampling or experimental design, reliable analytical methodologies and robust statistical analyses.
Although studies focusing on particular regions and target organisms are welcome, it is not the journal’s goal to publish essentially descriptive studies that provide results with narrow applicability, or are based on very small samples or pseudoreplication.
Rather, Biochemical Genetics welcomes review articles that go beyond summarizing previous publications and create added value through the systematic analysis and critique of the current state of knowledge or by conducting meta-analyses.
Methodological articles are also within the scope of Biological Genetics, particularly when new laboratory techniques or computational approaches are fully described and thoroughly compared with the existing benchmark methods.
Biochemical Genetics welcomes articles on the following topics: Genomics; Proteomics; Population genetics; Phylogenetics; Metagenomics; Microbial genetics; Genetics and evolution of wild and cultivated plants; Animal genetics and evolution; Human genetics and evolution; Genetic disorders; Genetic markers of diseases; Gene technology and therapy; Experimental and analytical methods; Statistical and computational methods.
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