ArticleBiochimica et biophysica acta2014
Transcriptional activation of PRMT5 by NF-Y is required for cell growth and negatively regulated by the PKC/c-Fos signaling in prostate cancer cells.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Focus on Lactate and Lactylation Modification: The Potential Role in Ophthalmic Disease Treatment.International journal of molecular sciences · 2026Review
- Discovery of an ApoE4-targeted small-molecule SirT1 enhancer for the treatment of Alzheimer's disease.Scientific reports · 2025Article
- PRMT5, regulated by lncRNA ZFAS1/miR-150-5p, promoted androgen-independent prostate cancer migration and invasion.Archives of medical science : AMS · 2025Article
- PRMT5 Mediated HIF1α Signaling and Ras-Related Nuclear Protein as Promising Biomarker in Hepatocellular Carcinoma.Biology · 2024Article
- WDR77 inhibits prion-like aggregation of MAVS to limit antiviral innate immune response.Nature communications · 2023Article
- Discovery and Biological Characterization of PRMT5:MEP50 Protein-Protein Interaction Inhibitors.Journal of medicinal chemistry · 2022Article
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- Reprogramming landscape highlighted by dynamic transcriptomes in therapy-induced neuroendocrine differentiation.Computational and structural biotechnology journal · 2022Article
- Sequential targeting of YAP1 and p21 enhances the elimination of senescent cells induced by the BET inhibitor JQ1.Cell death & disease · 2021Article
- PRMT5 function and targeting in cancer.Cell stress · 2020Review
- PRMT5-TRIM21 interaction regulates the senescence of osteosarcoma cells by targeting the TXNIP/p21 axis.Aging · 2020Article
- Combination BET Family Protein and HDAC Inhibition Synergistically Elicits Chondrosarcoma Cell Apoptosis Through RAD51-Related DNA Damage Repair.Cancer management and research · 2020Article
- Age-related difference in protective effect of early post-conditioning on ischemic brain injury: possible involvement of MAP-2/Synaptophysin role.Metabolic brain disease · 2019Article
- Curcumin ameliorates PRMT5-MEP50 arginine methyltransferase expression by decreasing the Sp1 and NF-YA transcription factors in the A549 and MCF-7 cells.Molecular and cellular biochemistry · 2019Article
- NF-YA transcriptionally activates the expression of SOX2 in cervical cancer stem cells.PloS one · 2019Article
- Recent advances in targeting protein arginine methyltransferase enzymes in cancer therapy.Expert opinion on therapeutic targets · 2018Review
- The PRMT5/WDR77 complex regulates alternative splicing through ZNF326 in breast cancer.Nucleic acids research · 2017Article
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- Inhibition of PKCα reduces the ability of migration of kidney cancer cells but has no impact on cell apoptosis.Experimental and therapeutic medicine · 2017Article
- Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Protein arginine methyltransferase 5 (PRMT5) symmetrically methylates arginine residues of histones and non-histone protein substrates and regulates a variety of cellular processes through epigenetic control of target gene expression or post-translational modification of signaling molecules. Recent evidence suggests that PRMT5 may function as an oncogene and its overexpression contributes to the development and progression of several human cancers. However, the mechanism underlying the regulation of PRMT5 expression in cancer cells remains largely unknown. In the present study, we have mapped the proximal promoter of PRMT5 to the -240bp region and identified nuclear transcription factor Y (NF-Y) as a critical transcription factor that binds to the two inverted CCAAT boxes and regulates PRMT5 expression in multiple cancer cell lines. Further, we present evidence that loss of PRMT5 is responsible for cell growth inhibition induced by knockdown of NF-YA, a subunit of NF-Y that forms a heterotrimeric complex with NF-YB and NF-YC for function. Significantly, we have found that activation of protein kinase C (PKC) by phorbol 12-myristate 13-acetate (PMA) in LNCaP prostate cancer cells down-regulates the expression of NF-YA and PRMT5 at the transcription level in a c-Fos-dependent manner. Given that down-regulation of several PKC isozymes is implicated in the development and progression of several human cancers, our findings suggest that the PKC-c-Fos-NF-Y signaling pathway may be responsible for PRMT5 overexpression in a subset of human cancer patients.
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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.