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Cellular assays evaluated proliferation, cell cycle progression, apoptosis, and invasion, with in vivo confirmation using a mouse subcutaneous xenograft model.",{"@graph":14,"@context":73},[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/research-report/","Research & 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ACCESS   \nFAM3C Regulates Glioma Cell Proliferation, Invasion, Apoptosis, and Epithelial Mesenchymal Transition via the Notch Pathway  \nXiaochao Xia  | Zihao Wang | Lvmeng Song | Yinchuan Cheng | Ping Xiong | Shun Li  \nDepartments of Neurosurgery, Affiliated Hospital of North Sichuan Medical College, Nanchong, China Correspondence: Shun Li ([morelee@163.com](morelee@163.com))  \nReceived: 11 March 2024 | Revised: 19 October 2024 | Accepted: 30 October 2024  \nFunding: The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This study was funded by the Sichuan Medical Science and Technology Innovation Research Association (YCH-KY-YCZD2024-054), the Affiliated Hospital of North Sichuan Medical College of China (2019ZD001), the North Sichuan Medical College (CBY23-ZDA01), and the Bureau of Science and Technology Nanchong City (19SXHZ0321) .  \nKeywords: epithelial mesenchymal transition | FAM3C | glioma | Notch pathway | therapeutic targets  \nABSTRACT  \nBackground: Previous studies have implicated the involvement of FAM3C in cancerous development and progression. Herein, we aimed to further investigate the oncological mechanism of FAM3C, specifically in glioma.  \nMethods: We utilized open-source bioinformatics tools and platforms to analyze the transcriptional expression levels, prognosis, and correlation with clinical variables of FAM3C in gliomas, and subsequently, to hypothesize its potential molecular functions and possibly associated signaling pathways. Following this, glioma tissues were obtained from resected specimens of patients to assess the expression of FAM3C and molecular markers related to epithelial–mesenchymal transition (EMT) and Notch signaling pathways. Furthermore, glioma cell lines were subjected to treatments including FAM3C siRNA knockdown, lentiviral overexpression, and Notch signaling pathway blockade, enabling the investigation of molecular functions of FAM3C in vitro, particularly in EMT and Notch signaling pathways, as well as its effects on cancer cell proliferation, cell cycle progression, apoptosis, and invasion, using assays such as MMT cell proliferation assay, transwell migration, and flow cytometry analysis. Finally, a mouse subcutaneous xenograft model was established to explore the integrative function ofFAM3C in glioma growth in vivo. Results: The expression level ofFAM3C correlated with the progression of glioma grade and served as a prognostic indicator for poor patient outcomes. Subsequent experiments conducted on glioma cell lines, tumor tissues, and mouse models reinforced the close association of FAM3C with processes including glioma cell proliferation, cell cycle progression, apoptosis, and invasion. Additionally, it was observed that FAM3C is involved in the regulation of the Notch signaling pathway.  \nConclusions: FAM3C emerges as a potential candidate for clinical detection and prognostic biomarker application. Its regulatory role in glioma cell proliferation, cell cycle progression, and modulation of epithelial–mesenchymal transition-driven invasion and migration via the Notch signaling pathway implies its potential to unveil novel therapeutic targets for glioma treatment.  \n1 | Introduction  \nGliomas, particularly glioblastoma (GBM), stand as the predominant primary malignancy within the human central nervous  \nsystem [1] . Currently, the standard treatment modalities for this pathology have primarily relied on surgical resection combined with postoperative radiotherapy, with or without temozolomide. Nonetheless, the clinical challenges of rapid invasion, metastasis,  \nThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.  \n© 2024 The Author(s). Cancer Medicine published by John Wiley & Sons Ltd.  \nCancer Medicine, 2024; 1","cbCaiumnypI1foaH","https://ap.wps.com/l/cbCaiumnypI1foaH","pdf",5946921,13,"English","# Abstract\n## Background\n## Methods\n## Results\n## Conclusions\n# Introduction","[{\"question\":\"What was the study’s main goal regarding FAM3C in glioma?\",\"answer\":\"To clarify the oncological mechanism of FAM3C in glioma and determine its involvement in EMT and Notch signaling-related processes.\"},{\"question\":\"How did the researchers test FAM3C’s function experimentally?\",\"answer\":\"They combined bioinformatics with measurements in patient glioma tissues and in vitro manipulation of glioma cell lines using FAM3C siRNA knockdown, lentiviral overexpression, and Notch pathway blockade.\"},{\"question\":\"What outcomes were associated with FAM3C in glioma?\",\"answer\":\"FAM3C expression correlated with glioma grade and poorer prognosis, and it was linked to proliferation, cell cycle progression, apoptosis, and invasion through regulation of the Notch signaling pathway.\"}]","FAM3C Regulates Glioma Cell Proliferation, Invasion, Apoptosis, and Epithelial Mesenchymal Transition via the Notch Pathway - Research Article | PDF",1789994251,33]