ArticleCancer research2019
PGC1α Inhibits Polyamine Synthesis to Suppress Prostate Cancer Aggressiveness.
Article in Cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 44 citations in OpenAlex.
- PGC1α-mediated upregulation of PHD2 represses HIF-signaling, limiting prostate cancer progression.Cell death and differentiation · 2026Article
- NNMT Loss Drives Cancer Progression by enhancing SAM availability for mTORC1 Signaling and Chromatin Methylation.bioRxiv : the preprint server for biology · 2026Article
- Hypusination of the translation factor eIF5A regulates mitochondrial tRNA processing to promote prostate cancer aggressiveness.Nature communications · 2026Article
- ODC1 Polyamine Metabolism Drives Prostate Cancer via AKT and Splicing.Journal of cellular and molecular medicine · 2026Article
- Metabolic reprogramming in cancer: signaling pathways and therapeutic targets.Molecular cancer · 2026Review
- Nanoparticle-mediated targeting of PGC-1α reveals critical metabolic pathways in bladder cancer metastasis.Communications biology · 2025Article
- Secreted spermidine synthase reveals a paracrine role for PGC1α-induced growth suppression in prostate cancer.Cell death & disease · 2025Article
- Role of PGC-1α in the proliferation and metastasis of malignant tumors.Journal of molecular histology · 2025Review
- Prokaryotic organelle mitochondria drive tumorigenesis: "the original sin".Frontiers in oncology · 2025Review
- Molecular subtyping and functional characterization of gastric cancer using arginine metabolism-related genes.Frontiers in cell and developmental biology · 2025Article
- Prognostic, oncogenic roles, and pharmacogenomic features of AMD1 in hepatocellular carcinoma.Cancer cell international · 2024Article
- PGC-1α drives small cell neuroendocrine cancer progression toward an ASCL1-expressing subtype with increased mitochondrial capacity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Metabolic adaptations in prostate cancer.British journal of cancer · 2024Review
- Metabolomic profiling of cancer-related fatigue involved in cachexia and chemotherapy.Scientific reports · 2024Article
- Peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family in physiological and pathophysiological process and diseases.Signal transduction and targeted therapy · 2024Review
- From metabolism to malignancy: the multifaceted role of PGC1α in cancer.Frontiers in oncology · 2024Review
- Polyamines: their significance for maintaining health and contributing to diseases.Cell communication and signaling : CCS · 2023Review
- Hypoxia-responsive PPARGC1A/BAMBI/ACSL5 axis promotes progression and resistance to lenvatinib in hepatocellular carcinoma.Oncogene · 2023Article
- Mitochondrial Alterations in Prostate Cancer: Roles in Pathobiology and Racial Disparities.International journal of molecular sciences · 2023Review
- One-Carbon and Polyamine Metabolism as Cancer Therapy Targets.Biomolecules · 2022Review
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 4 countries.
Funding
Abstract
Although tumorigenesis is dependent on the reprogramming of cellular metabolism, the metabolic pathways engaged in the formation of metastases remain largely unknown. The transcriptional coactivator peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) plays a pleiotropic role in the control of cancer cell metabolism and has been associated with a good prognosis in prostate cancer. Here, we show that PGC1α represses the metastatic properties of prostate cancer cells via modulation of the polyamine biosynthesis pathway. Mechanistically, PGC1α inhibits the expression of c-MYC and ornithine decarboxylase 1 (ODC1), the rate-limiting enzyme for polyamine synthesis. Analysis of
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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.