ArticleCellular and molecular neurobiology2023
Cell Cycle-Related FAM64A Could be Activated by TGF-β Signaling to Promote Glioma Progression.
Article in Cellular and molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Targeting FAM64A: a promising strategy to halt liver cancer angiogenesis and enhance immunity.American journal of cancer research · 2026Article
- Targeting TGF-β signaling in glioblastoma: therapeutic implications and novel drug development strategies.Brain tumor pathology · 2025Review
- FAM64A silencing inhibits the proliferation, migration, invasion, and epithelial-mesenchymal transition in ovarian cancer cells via activating Hippo pathway.Discover oncology · 2025Article
- Deciphering the prognostic significance of WDR77 in gliomas: a comprehensive analysis.Scientific reports · 2025Article
- Oncogenic role and prognostic significance of PIMREG in melanoma.Translational cancer research · 2025Article
- FAM64A regulates the malignant phenotype and tumor microenvironment of non-small cell lung cancer by activating the JAK/STAT3/PDL1 axis.Journal of molecular histology · 2025Article
- Knockout of the ING5 epigenetic regulator confirms roles in stem cell maintenance and tumor suppression in vivo.PloS one · 2025Article
- Disclosing transcriptomics network-based signatures of glioma heterogeneity using sparse methods.BioData mining · 2023Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Gliomas are aggressive brain tumors characterized by uncontrolled cell proliferation. FAM64A, a cell cycle-related gene, has been found to promote cell proliferation in various tumors, including gliomas. However, the regulatory mechanism and clinical significance of FAM64A in gliomas remain unclear. In this study, we investigated FAM64A expression in gliomas with different grades and constructed FAM64A silenced cell lines to study its functions. Our results demonstrated that FAM64A was highly expressed in glioblastoma (P < 0.001) and associated with a poor prognosis (P < 0.001). Expression profiles at the single-cell resolution indicated FAM64A could play a role in a cell-cycle-dependent way to promote glioma cell proliferation. We further observed that FAM64A silencing in glioma cells resulted in disrupted proliferation and migration ability, and increased cell accumulation in the G2/M phase (P = 0.034). Additionally, TGF-β signaling upregulates FAM64A expression, and SMAD4 and FAM64A co-localize in high-grade glioma tissues. We found FAM64A knockdown inhibited TGF-β-induced epithelial-mesenchymal transition in glioma. Our findings suggest that FAM64A could serve as a diagnostic and therapeutic target in gliomas.
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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 OpenQuestion graph.