Ask about this productRelated genes to: FAM3C Blocking Peptide
- Gene:
- FAM3C NIH gene
- Name:
- family with sequence similarity 3 member C
- Previous symbol:
- -
- Synonyms:
- GS3876, ILEI
- Chromosome:
- 7q31.31
- Locus Type:
- gene with protein product
- Date approved:
- 2002-06-18
- Date modifiied:
- 2016-10-05
Related products to: FAM3C Blocking Peptide
Related articles to: FAM3C Blocking Peptide
- Cancers reprogram their metabolism to provide anabolic needs without driving excessive oxidative stress. Attention has focused on glucose metabolism, yet amino acid synthesis and degradation also promote tumor cell states and growth. Here, we assessed amino acids that maintain cancer stem cells in glioblastoma and found increased proline levels relative to differentiated tumor progeny through increased proline synthesis. Cancer stem cells preferentially expressed the signaling molecule FAM3C induced by the stem cell transcription factor SOX2 to drive expression of proline synthesis enzymes. FAM3C classically mediated cellular responses as a secreted protein but gained intracellular functions in cancer stem cells through binding the histone reader spindlin 1 (SPIN1), thereby preventing its lysosomal degradation, assisting its nuclear localization, and promoting epigenetic regulation of proline synthesis. Proline synthesis depleted ROS, and genetic targeting of FAM3C attenuated ROS scavenging, whereas SPIN1 OE restored ROS levels. Molecular docking identified tucatinib as a brain-penetrant pharmacologic disruptor of FAM3C-SPIN1 interactions, promoting SPIN1 degradation and reducing intracellular proline levels. Thus, cancer stem cells induced a favorable metabolic state through proline synthesis and ROS depletion, revealing potential therapeutic dependencies. - Source: PubMed
Publication date: 2026/06/01
Wu WeichiZhang PoWang DonghaiWu XujiaWu QiulianLi DaqiHuang TengfeiWang RuiLi HuanMi HailongTaori SuchetYuan FanenDuan TingtingChen ZhiyeYuan HuairuiRich Jeremy N - This study comprehensively investigated the role of FAM3 family genes (, , , ) in Kidney Renal Clear Cell Carcinoma (KIRC) using an integrative multi-dimensional approach. Analyses included mRNA expression profiling, promoter methylation assessment, genetic alteration evaluation, prognostic modeling, immune and molecular subtype correlations, gene enrichment analysis, in vitro functional validation, and drug sensitivity evaluation based on TCGA datasets and experimental data. Expression analysis revealed significant upregulation of and and downregulation of and in KIRC tissues compared with normal kidney samples. ROC curve analysis demonstrated their diagnostic potential. Promoter methylation analysis indicated hypomethylation of and and hypermethylation of and , consistent with their expression profiles. Minimal genetic alterations were observed, suggesting that epigenetic regulation may primarily contribute to their dysregulation. Prognostic modeling associated gene expression with overall survival, indicating their potential as predictive biomarkers. Immune infiltration and subtype analyses suggested that genes are involved in the modulation of the tumor microenvironment. Functional validation demonstrated that knockdown of and suppressed cell proliferation and colony formation, while enhancing migratory and wound-healing abilities in KIRC cell lines. Drug sensitivity analysis identified correlations between expression and responsiveness to anticancer compounds. These findings highlight the diagnostic, prognostic, and therapeutic significance of family genes in KIRC, providing valuable insights for future clinical translation and potential targeted therapy development. - Source: PubMed
Publication date: 2026/05/06
Zhe WangAbbas MuhammadAbdel-Maksoud Mostafa AAlmanaa Taghreed NAlmutair SaeedahAlamri AbdulazizAufy MohammedAl-Qahtani Wahidah HHameed Yasir - Diabetes affects >500 million people worldwide. Despite insulin therapy, most patients develop devastating complications, emphasizing the need for curative strategies. Human multipotent stromal/stem cells (MSC) secrete factors that promote islet regeneration. We previously showed that intrapancreatic (iPan) delivery of Wnt-activated MSC-conditioned media (Wnt+ CM) stimulates islet regeneration without cell transfer. This study aimed to identify and functionally validate specific MSC-secreted proteins with islet regenerative potential. - Source: PubMed
Xie Xin YAl-Banaa Nouran NTian YinaBell Gillian IKuljanin MiljanCooper Tyler TPodgers Caleb JSharma AjayaXenocostas AnargyrosLajoie Gilles AHess David A - Epithelial-mesenchymal transition (EMT) is a key driver of invasion, metastasis, and treatment resistance in gastric cancer, yet its post-transcriptional regulation by microRNAs (miRNAs) is not fully delineated. We performed a structured literature search in PubMed, Web of Science, and Scopus for studies evaluating miRNAs in relation to EMT in gastric cancer and synthesised tumor-intrinsic, microenvironmental, and circulating EMT-related miRNA networks. Downregulated, predominantly tumor-suppressive miRNAs, including miR-34a, miR-200 family, miR-148a, miR-204, miR-30a, miR-101, miR-218, miR-26a, miR-375, miR-506, and others, converge on EMT transcription factors and pathways such as ZEB1/2, Snail, TGF-β/SMAD, Wnt/β-catenin, c-Met, and PI3K/AKT, and their restoration reverses EMT phenotypes in preclinical models. Upregulated oncomiRs, such as miR-21, miR-17-5p, miR-106b-5p, miR-23a, miR-130a-3p, miR-196a-5p, miR-181a, miR-616-3p, miR-301a-3p, miR-150, miR-27a-3p and miR-192/215, target tumor suppressors and reinforce these pathways. Cancer-associated fibroblast, macrophage, neutrophil, and natural killer cell-derived miRNAs, together with systemic indices such as the neutrophil-to-lymphocyte ratio and mediators like FAM3C, add microenvironmental layers of EMT regulation. Several EMT-related miRNAs show consistent associations with invasion, metastasis, peritoneal dissemination, prognosis, and chemoresistance, and many are detectable in circulation. Overall, EMT-related miRNAs orchestrate gastric cancer cell plasticity and tumor-microenvironment crosstalk and represent promising biomarker and therapeutic candidates that warrant validation in prospective, subtype-stratified, and translational studies. - Source: PubMed
Publication date: 2026/01/30
Biskupski MaciejBrachet AdamHunek GabrielaKarabin AgnieszkaCzerski MichałBojarska WiktoriaKarpiński RobertTeresiński GrzegorzForma AlicjaBaj Jacek - Type 2 diabetes complications manifest across various organs, but are fundamentally rooted in vascular dysfunction. This study aims to identify plasma protein signatures that improve prediction of macrovascular and microvascular complications in type 2 diabetes over classical clinical factors, assess the stability of their prognostic performance over time, and explore the cross-ancestry generalizability of the developed models. - Source: PubMed
Publication date: 2026/01/20
Huang YueTutino MauroSingh ArchitRayner Nigel WilliamBarysenka AndreiBocher OzvanZeggini Eleftheria