The p53 tumor suppressor gene has recently been shown to mediate metabolic changes in cells under physiological and pathological conditions. It has been revealed that p53 regulates energy metabolism, oxidative stress, and amino acid metabolism through balancing glycolysis and oxidative phosphorylation (OXPHOS) as well as the autophagy pathway. p53 is activated by metabolic stress through AMP-activated protein kinase (AMPK) and the mammalian target of rapamycin (mTOR) signaling pathways. p53 regulates OXPHOS through the transcriptional regulation of fructose-2,6-bisphosophatase, TP53-induced glycolysis regulator (TIGAR) and synthesis of cytochrome c oxidase (SCO2) subunit of complex IV of the electron transport chain. p53 also indirectly influences the energy metabolism through regulating glucose transporter (GLUT) expression, glutaminase 2 (GLS2) and fatty acid synthase (FAS). In addition, p53 regulates autophagy to provide cell metabolites for surviving through damage regulated autophagy modulator (DRAM1). Here we review the recent findings to elucidate the important role of p53 in cell metabolism.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4002322 | PMC |
| http://dx.doi.org/10.1038/aps.2010.151 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Natural products and long non-coding RNAs in prostate cancer: insights into etiology and treatment resistance.
Naunyn Schmiedebergs Arch Pharmacol
January 2025
Department of Biochemistry, Faculty of Pharmacy, Badr University in Cairo (BUC), Badr City, , 11829, Cairo, Egypt.
Globally, the incidence and death rates associated with cancer persist in rising, despite considerable advancements in cancer therapy. Although some malignancies are manageable by a mix of chemotherapy, surgery, radiation, and targeted therapy, most malignant tumors either exhibit poor responsiveness to early identification or endure post-treatment survival. The prognosis for prostate cancer (PCa) is unfavorable since it is a perilous and lethal malignancy.
View Article and Find Full Text PDFInteraction of STIL with FOXM1 regulates SF3A3 transcription in the hepatocellular carcinoma development.
Cell Div
January 2025
Second Department of General Surgery, the First Hospital of Qiqihar, No. 700, Pukui avenue, Long sha District, Qiqihar, Heilongjiang, 161000, P. R. China.
Background: Dysregulation of SF3A3 has been related to the development of many cancers. Here, we investigated the functional role of SF3A3 in hepatocellular carcinoma (HCC).
Methods: SF3A3 expression in HCC tissues and cell lines was examined using RT-qPCR.
Knockdown of CNOT3, a subunit of the CCR4-NOT deadenylase complex, sensitizes A549 human non-small cell lung cancer cells to senescence-inducing stimuli.
Biochem Biophys Res Commun
January 2025
Membranology Unit, Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha, Onna, Okinawa, 904-0495, Japan. Electronic address:
Cellular senescence is an essentially irreversible cell cycle arrest associated with upregulated inflammatory responses that contribute to various pathological and physiological processes, including aging, cancer, and cancer prevention. However, the underlying mechanisms are not fully understood. Here, we show that the downregulation of CNOT3, a subunit of the CCR4-NOT complex that deadenylates mRNA poly(A) tails, promotes cellular senescence in subpopulation of A549 human non-small cell lung cancer cells.
View Article and Find Full Text PDFNanosize Non-Viral Gene Therapy Reverses Senescence Reprograming Driven by PBRM1 Deficiency to Suppress iCCA Progression.
Adv Sci (Weinh)
January 2025
Department of Hepatic Surgery, Center of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China.
Polybromo-1 (PBRM1) serves as a crucial regulator of gene transcription in various tumors, including intrahepatic cholangiocarcinoma (iCCA). However, the exact role of PBRM1 in iCCA and the mechanism by which it regulates downstream target genes remain unclear. This research has revealed that PBRM1 is significantly downregulated in iCCA tissues, and this reduced expression is linked to aggressive clinicopathological features and a poor prognosis.
View Article and Find Full Text PDFIron metabolism in a mouse model of hepatocellular carcinoma.
Sci Rep
January 2025
Institute of Comparative Molecular Endocrinology, Ulm University, 89081, Ulm, Germany.
Hepatocellular carcinoma (HCC) remains the most prevalent type of primary liver cancer worldwide. p53 is one of the most frequently mutated tumor-suppressor genes in HCC and its deficiency in hepatocytes triggers tumor formation in mice. To investigate iron metabolism during liver carcinogenesis, we employed a model of chronic carbon tetrachloride injections in liver-specific p53-deficient mice to induce liver fibrosis, cirrhosis and subsequent carcinogenesis.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!