ArticleOncotarget2016
Phosphorylation of PPARγ at Ser84 promotes glycolysis and cell proliferation in hepatocellular carcinoma by targeting PFKFB4.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Nanoparticle-Mediated PPAR Modulation of Macrophage Polarization in Radiation Enteritis: A Narrative Review.Drug design, development and therapy · 2026Review
- Article
- Melatonin inhibits bladder tumorigenesis by suppressing PPARγ/ENO1-mediated glycolysis.Cell death & disease · 2023Article
- In vivo study revealed pro-tumorigenic effect of CMTM3 in hepatocellular carcinoma involving the regulation of peroxisome proliferator-activated receptor gamma (PPARγ).Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Integrated investigation and experimental validation of PPARG as an oncogenic driver: implications for prognostic assessment and therapeutic targeting in hepatocellular carcinoma.Frontiers in pharmacology · 2023Article
- Integrative analysis of mitochondrial metabolic reprogramming in early-stage colon and liver cancer.Frontiers in oncology · 2023Article
- Can PPARBiomolecules · 2022Article
- PFKFB4 interacts with ICMT and activates RAS/AKT signaling-dependent cell migration in melanoma.Life science alliance · 2022Article
- Pathophysiological Mechanisms in Non-Alcoholic Fatty Liver Disease: From Drivers to Targets.Biomedicines · 2021Review
- Hepatocarcinogenesis Prevention by Pirfenidone Is PPARγ Mediated and Involves Modification of Nuclear NF-kB p65/p50 Ratio.International journal of molecular sciences · 2021Article
- PFKFB4 as a promising biomarker to predict a poor prognosis in patients with gastric cancer.Oncology letters · 2021Article
- A nomogram combining PPARγ expression profiles and clinical factors predicts survival in patients with hepatocellular carcinoma.Oncology letters · 2021Article
- PFKFB4 promotes lung adenocarcinoma progression via phosphorylating and activating transcriptional coactivator SRC-2.BMC pulmonary medicine · 2021Article
- Review
- Long noncoding RNA FIRRE contributes to the proliferation and glycolysis of hepatocellular carcinoma cells by enhancing PFKFB4 expression.Journal of Cancer · 2021Article
- Competitive glucose metabolism as a target to boost bladder cancer immunotherapy.Nature reviews. Urology · 2020Review
- Analysis of Key Genes Regulating the Warburg Effect in Patients with Gastrointestinal Cancers and Selective Inhibition of This Metabolic Pathway in Liver Cancer Cells.OncoTargets and therapy · 2020Article
- Immunometabolic modulation of retinal inflammation by CD36 ligand.Scientific reports · 2019Article
- Review
- 6-Phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 and 4: A pair of valves for fine-tuning of glucose metabolism in human cancer.Molecular metabolism · 2019Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peroxisome proliferator-activating receptor γ (PPARγ), a transcription factor, is involved in many important biological processes, including cell terminal differentiation, survival and apoptosis. However, the role of PPARγ, which regulates tumour promoter and oncogene expression, is not well understood in hepatocellular carcinoma (HCC). In the present study, based on evidence from clinical samples that phosphorylation of PPARγ at Ser84 is up-regulated in human liver tumours, we confirmed that phosphorylation of PPARγ was also significantly increased in an HCC mouse model and was increased by Mitogen-activated protein kinase (MEK)/ Extracellular-signal-regulated kinases (ERK) kinase. Next, we performed an RNA microarray analysis, and our data indicated that dephosphorylation of PPARγ at Ser84 affects the expression of glycolysis-related genes and pro-proliferation genes, which supposedly promote proliferation of HCC cells. Using a chromatin immunoprecipitation (ChIP) assay, we demonstrated that the observed PPARγ-mediated induction of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4 (PFKFB4) expression was directly modulated by the transcriptional activity of its promoter. Furthermore, using knockdown of PFKFB4, we elucidated that the stimulation of PPARγ phosphorylation on glycolysis and proliferation in HCC is dependent on PFKFB4. Together, these findings extend our understanding of how liver tumour cells reprogram their glycolytic pathways by post-translational modification of specific transcription factors and lay a foundation for the screening of new targets for the treatment of HCC.
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