ArticleCell research2018
KRAB-type zinc-finger proteins PITA and PISA specifically regulate p53-dependent glycolysis and mitochondrial respiration.
Article in Cell research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- Mitochondrial metabolite transporters at the crossroads of metabolic reprogramming, epigenetic regulation and therapeutic vulnerabilities in colorectal cancer.Molecular biology reports · 2026Review
- KRAB Zinc-Finger Protein ZNF205 Promotes Hepatocellular Carcinoma via p53 Pathway Repression.Cancer science · 2026Article
- Bulk and Single-Cell Transcriptomics Reveal That SCO2 Drives Psoriasis via Activating CCR7International journal of molecular sciences · 2026Article
- The Interdependence of Carbon Substrates and Metabolic Pathways Enables the Metabolic Plasticity of Cancer Cells.Advances in experimental medicine and biology · 2026Review
- p53-mediated regulation of electron transport chain and nucleotide synthesis during Newcastle disease virus infection.Journal of virology · 2025Article
- ZNF280A promotes malignant melanoma development through regulating cell proliferation, apoptosis, and cell cycle.Discover oncology · 2025Article
- Metabolic Targets in CRC: The Emerging Role of Cytochrome P450 Inhibitors.Current pharmaceutical design · 2025Review
- Role of glucose metabolic reprogramming in colorectal cancer progression and drug resistance.Translational oncology · 2024Review
- Chrysophanol inhibits of colorectal cancer cell motility and energy metabolism by targeting the KITENIN/ErbB4 oncogenic complex.Cancer cell international · 2024Article
- Non-Coding RNAs of Mitochondrial Origin: Roles in Cell Division and Implications in Cancer.International journal of molecular sciences · 2024Review
- The Roles of Zinc Finger Proteins in Colorectal Cancer.International journal of molecular sciences · 2023Review
- METTL14 modulates glycolysis to inhibit colorectal tumorigenesis in p53-wild-type cells.EMBO reports · 2023Article
- The p52-ZER6/G6PD axis alters aerobic glycolysis and promotes tumor progression by activating the pentose phosphate pathway.Oncogenesis · 2023Article
- Metabolic reprogramming in colorectal cancer: regulatory networks and therapy.Cell & bioscience · 2023Review
- Article
- ZNF498 promotes hepatocellular carcinogenesis by suppressing p53-mediated apoptosis and ferroptosis via the attenuation of p53 Ser46 phosphorylation.Journal of experimental & clinical cancer research : CR · 2022Article
- Deoxyribonuclease 1-like 3 Inhibits Hepatocellular Carcinoma Progression by Inducing Apoptosis and Reprogramming Glucose Metabolism.International journal of biological sciences · 2022Article
- Downregulation of ZNF280A inhibits proliferation and tumorigenicity of colorectal cancer cells by promoting the ubiquitination and degradation of RPS14.Frontiers in oncology · 2022Article
- Article
- Genetic and biological hallmarks of colorectal cancer.Genes & development · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Few p53 regulators participate in selective control of p53-mediated cellular metabolism. How p53-mediated aerobic and glycolytic pathways are negatively regulated remains largely unclear. Here, we identified two KRAB-type zinc-finger proteins, PITA (p53 inhibitor of TIGAR activation) and PISA (p53 inhibitor of SCO2 activation), as selective regulators of p53 in metabolic control. PITA and PISA interact with p53 and specifically suppress transcription of the glycolysis regulator TIGAR and the oxidation phosphorylation regulator SCO2, respectively. Importantly, PITA transgenic mice exhibited increased 6-phosphofructokinase 1 (PFK1) activity and an elevated glycolytic rate, whereas PISA transgenic mice had decreased cytochrome c oxidase activity and reduced mitochondrial respiration. In response to glucose starvation, PITA dissociates from p53, resulting in activation of p53 and induction of TIGAR, which inhibited aerobic glycolysis. Prolonged starvation leads to PISA dissociation from p53 and induction of SCO2 and p53-promoted mitochondrial respiration. The dynamic regulation of PITA and PISA upon metabolic stress is dependent on ATM kinase-mediated phosphorylation of PITA and PISA. Furthermore, in human colorectal cancers, the elevated expression of PITA and PISA correlates with cancer progression. Depletion of PITA or PISA in colorectal cancer cells reduced the cell proliferation, migration and invasion. These results identify PITA and PISA as selective regulators of p53-mediated glycolysis and mitochondrial respiration and provide novel insights into the role of p53 network in cell metabolic control.
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