ArticleCancer medicine2024
FAM3C Regulates Glioma Cell Proliferation, Invasion, Apoptosis, and Epithelial Mesenchymal Transition via the Notch Pathway.
Article in Cancer medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Cancer stem cells synthesize proline to attenuate oxidative stress.The Journal of clinical investigation · 2026Article
- The central role of EMT in tumor progression: mechanistic drivers, biomarker discovery, and therapeutic horizons.Frontiers in pharmacology · 2026Review
- The roles, signalling pathways and therapeutic implications of Apoc1 in cancer.Discover oncology · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundPrevious 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.
methodsWe 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 of FAM3C in glioma growth in vivo.
resultsThe expression level of FAM3C 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.
conclusionsFAM3C 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.