NDLI: p53 promotes the expression of gluconeogenesis-related genes and enhances hepatic glucose production

Content Provider	Springer Nature : BioMed Central
Author	Goldstein, Ido Yizhak, Keren Madar, Shalom Goldfinger, Naomi Ruppin, Eytan Rotter, Varda
Abstract	Background The p53 tumor suppressor protein is a transcription factor that initiates transcriptional programs aimed at inhibiting carcinogenesis. p53 represses metabolic pathways that support tumor development (such as glycolysis and the pentose phosphate pathway (PPP)) and enhances metabolic pathways that are considered counter-tumorigenic such as fatty acid oxidation. Findings In an attempt to comprehensively define metabolic pathways regulated by p53, we performed two consecutive high-throughput analyses in human liver-derived cells with varying p53 statuses. A gene expression microarray screen followed by constraint-based modeling (CBM) predicting metabolic changes imposed by the transcriptomic changes suggested a role for p53 in enhancing gluconeogenesis (de novo synthesis of glucose). Examining glucogenic gene expression revealed a p53-dependent induction of genes involved in both gluconeogenesis (G6PC, PCK2) and in supplying glucogenic precursors (glycerol kinase (GK), aquaporin 3 (AQP3), aquaporin 9 (AQP9) and glutamic-oxaloacetic transaminase 1 (GOT1)). Accordingly, p53 augmented hepatic glucose production (HGP) in both human liver cells and primary mouse hepatocytes. Conclusions These findings portray p53 as a novel regulator of glucose production. By facilitating glucose export, p53 may prevent it from being shunted to pro-cancerous pathways such as glycolysis and the PPP. Thus, our findings suggest a metabolic pathway through which p53 may inhibit tumorigenesis.
Related Links	https://cancerandmetabolism.biomedcentral.com/counter/pdf/10.1186/2049-3002-1-9.pdf
Ending Page	6
Page Count	6
Starting Page	1
File Format	HTM / HTML
ISSN	20493002
DOI	10.1186/2049-3002-1-9
Journal	Cancer & Metabolism
Issue Number	1
Volume Number	1
Language	English
Publisher	BioMed Central
Publisher Date	2013-02-04
Access Restriction	Open
Subject Keyword	Cancer Research Oncology Metabolomics Metabolic Diseases Imaging Radiology Cell Biology p53 Gluconeogenesis Hepatic glucose production Diabetes
Content Type	Text
Resource Type	Article
Subject	Cancer Research
Journal Impact Factor	6/2023
5-Year Journal Impact Factor	5.4/2023

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

p53 promotes the expression of gluconeogenesis-related genes and enhances hepatic glucose production

Stratification of cancer and diabetes based on circulating levels of formate and glucose

Palmitoleate attenuates diet induced insulin resistance and hepatic inflammation independently of PPAR-α

Global metabolic alterations in colorectal cancer cells during irinotecan-induced DNA replication stress

The in vivo function of TIGAR, a p53 target gene that regulates glucose metabolism

Deficiency of TOP1MT enhances glycolysis through the stimulation of PDK4 expression in gastric cancer

Metabolic reprogramming by KSHV in cellular transformation

SIRT6 enhances oxidative phosphorylation in breast cancer and promotes mammary tumorigenesis in mice

Leucine supplementation differentially enhances pancreatic cancer growth in lean and overweight mice

p53 promotes the expression of gluconeogenesis-related genes and enhances hepatic glucose production

Similar Documents

p53 promotes the expression of gluconeogenesis-related genes and enhances hepatic glucose production

Stratification of cancer and diabetes based on circulating levels of formate and glucose

Palmitoleate attenuates diet induced insulin resistance and hepatic inflammation independently of PPAR-α

Global metabolic alterations in colorectal cancer cells during irinotecan-induced DNA replication stress

The in vivo function of TIGAR, a p53 target gene that regulates glucose metabolism

Deficiency of TOP1MT enhances glycolysis through the stimulation of PDK4 expression in gastric cancer

Metabolic reprogramming by KSHV in cellular transformation

SIRT6 enhances oxidative phosphorylation in breast cancer and promotes mammary tumorigenesis in mice

Leucine supplementation differentially enhances pancreatic cancer growth in lean and overweight mice

p53 promotes the expression of gluconeogenesis-related genes and enhances hepatic glucose production