ArticleCancer science2021
An AKT/PRMT5/SREBP1 axis in lung adenocarcinoma regulates de novo lipogenesis and tumor growth.
Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Clinicopathological and Prognostic Significance of PRMT5 in Cancers: A System Review and Meta-Analysis.Cancer control : journal of the Moffitt Cancer CenterPooled it
- Lipid Metabolic Reprogramming in Lung Cancer: Mechanisms and Therapeutic Targets in the Tumor Microenvironment.International journal of cancer · 2026Review
- Protein arginine methyltransferases as metabolic regulators: many roles beyond cancer.Science China. Life sciences · 2026Review
- PKC-iota drives EGFR-TKI resistance in EGFR-mutated NSCLC by phosphorylating FASN to reprogram lipid metabolism.Translational lung cancer research · 2026Article
- Protein arginine methyltransferase 5 as a novel therapeutic target in solid tumors.Genes & diseases · 2026Review
- Unveiling Metabolic Signatures as Potential Biomarkers in Common Cancers: Insights from Lung, Breast, Colorectal, Liver, and Gastric Tumours.Biomolecules · 2025Review
- Deciphering the role of IGF2BP2 and PRMT5 in gallbladder cancer progression: insights from multi-omics analysis.British journal of cancer · 2025Article
- Combined spatially resolved metabolomics and spatial transcriptomics reveal the mechanism of RACK1-mediated fatty acid synthesis.Molecular oncology · 2025Article
- Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025Review
- Xingxiao Pill Suppressed the Progression of Non-Small Cell Lung Cancer by Targeting SREBP1/FASN-Induced Fatty Acid Biosynthesis via PI3K/AKT/mTOR Signaling Pathway.Cancer management and research · 2025Article
- The roles and mechanisms of SREBP1 in cancer development and drug response.Genes & diseases · 2024Review
- Metabolic reprogramming in lung cancer and its clinical implication.Frontiers in pharmacology · 2024Review
- Nuclear PRMT5 is a biomarker of sensitivity to tamoxifen in ERαEMBO molecular medicine · 2023Article
- PRMT5 links lipid metabolism to contractile function of skeletal muscles.EMBO reports · 2023Article
- Prmt5 deficiency inhibits CD4+ T-cell Klf2/S1pr1 expression and ameliorates EAE disease.Journal of neuroinflammation · 2023Article
- PRMT5 inhibition induces pro-inflammatory macrophage polarization and increased hepatic triglyceride levels without affecting atherosclerosis in mice.Journal of cellular and molecular medicine · 2023Article
- USP7- and PRMT5-dependent G3BP2 stabilization drives de novo lipogenesis and tumorigenesis of HNSC.Cell death & disease · 2023Article
- Overview of Cancer Metabolism and Signaling Transduction.International journal of molecular sciences · 2022Review
- NSCLC Cells Resistance to PI3K/mTOR Inhibitors Is Mediated by Delta-6 Fatty Acid Desaturase (FADS2).Cells · 2022Article
- PTPRO represses colorectal cancer tumorigenesis and progression by reprogramming fatty acid metabolism.Cancer communications (London, England) · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Protein kinase B (AKT) hyperactivation and de novo lipogenesis are both common in tumor progression. Sterol regulatory element-binding protein 1 (SREBP1) is the master regulator for tumor lipid metabolism, and protein arginine methyltransferase 5 (PRMT5) is an enzyme that can catalyze symmetric dimethyl arginine (SDMA) modification of the mature form of SREBP1 (mSREBP1) to induce its hyperactivation. Here, we report that SDMA-modified mSREBP1 (mSREBP1-SDMA) was overexpressed and correlated with Ser473-phosphorylated AKT (AKT-473P) expression and poor patient outcomes in human lung adenocarcinomas. Furthermore, patients with AKT-473P and mSREBP1-SDMA coexpression showed the worst prognosis. Mechanistic investigation revealed that AKT activation upregulated SREBP1 at both the transcriptional and post-translational levels, whereas PRMT5 knockdown reversed AKT signaling-mediated mSREBP1 ubiquitin-proteasome pathway stabilization at the post-translational level. Meanwhile, AKT activation promoted nuclear PRMT5 to the cytoplasm without changing total PRMT5 expression, and the transported cytoplasmic PRMT5 (cPRMT5) induced by AKT activation showed a strong mSREBP1-binding ability. Immunohistochemical assay indicated that AKT-473P and mSREBP1-SDMA were positively correlated with cPRMT5 in lung adenocarcinomas, and high cPRMT5 levels in tumors were associated with poor patient outcomes. Additionally, PRMT5 knockdown reversed AKT activation-induced lipid synthesis and growth advantage of lung adenocarcinoma cells both in vitro and in vivo. Finally, we defined an AKT/PRMT5/SREBP1 axis involved in de novo lipogenesis and the growth of lung cancer. Our data also support that cPRMT5 is a potential therapeutic target for hyperactive AKT-driven lung adenocarcinoma.
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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.