ArticleEMBO reports2021
p53 transcriptionally regulates SQLE to repress cholesterol synthesis and tumor growth.
Article in EMBO reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- Squalene Epoxidase: Its Regulations and Links with Cancers.International journal of molecular sciences · 2024Pooled it
- Metabolites and cancer metastasis.Oncogene · 2026Review
- An EZH2-SREBP2 axis promotes cholesterol biosynthesis and represents a noncanonical vulnerability in tumorigenesis.Nature cell biology · 2026Article
- Targeting SQLE-Mediated Cholesterol Metabolism to Promote Oxidative Stress and Attenuate Drug Resistance in Osteosarcoma.Antioxidants (Basel, Switzerland) · 2026Article
- Prolonged high-dose prenatal caffeine exposure induces organ-specific developmental toxicity: renal p53 downregulation and hepatic caspase-3 upregulation in neonatal mice, supported with in silico studies.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Metabolic Adaptation and Potential Regulatory Mechanisms of Longissimus Dorsi-Derived Skeletal Muscle Satellite Cells from Hu Sheep Under Insulin Induction.Animals : an open access journal from MDPI · 2026Article
- Rethinking residual p53 function in HPV-positive cervical cancer cells.Journal of virology · 2026Article
- Noncanonical PI(4,5)PScience advances · 2026Article
- Farnesyltransferase Deficiency in Cardiomyocytes Initiates Senescence and Contributes to Cardiac Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting cholesterol-driven immunometabolism in cancer: from molecular circuits to clinical translation.Molecular cancer · 2026Review
- Cholesterol Metabolism-related Characteristics Predict Therapeutic Response and Survival in Esophageal Cancer.Journal of advanced research · 2026Article
- Integrated Bioinformatics Analysis Revealing that the NSDHL Gene Might Be Associated with the Progression of Western HFD/SW-Induced Hepatocellular CarcinomaEndocrine, metabolic & immune disorders drug targets · 2026Article
- Cholesterol metabolic rewiring shapes immune remodeling across hepatocarcinogenesis.Frontiers in immunology · 2026Review
- Noncoding RNAs in Metabolic Reprogramming of Breast Cancer: Dietary Opportunities and Translational Implications.Experientia supplementum (2012) · 2026Review
- Advanced multifunctional nano-delivery platform focusing on treating diseases related to lipid metabolism via targeted intervention in various lipid metabolic processes.Military Medical Research · 2025Review
- Relationship between Abnormal Lipid Metabolism and Gallstone Formation.The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi · 2025Review
- Advances in the role of the IGF signaling system in myelodysplastic syndromes and acute myeloid leukemia.Frontiers in oncology · 2025Review
- Article
- Mechanism and therapeutic potential of liver injury induced by cholesterol-associated proteins.Frontiers in pharmacology · 2025Review
- Stabilization of SQLE mRNA by WTAP/FTO/IGF2BP3-dependent manner in HGSOC: implications for metabolism, stemness, and progression.Cell death & disease · 2024Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cholesterol is essential for membrane biogenesis, cell proliferation, and differentiation. The role of cholesterol in cancer development and the regulation of cholesterol synthesis are still under active investigation. Here we show that under normal-sterol conditions, p53 directly represses the expression of SQLE, a rate-limiting and the first oxygenation enzyme in cholesterol synthesis, in a SREBP2-independent manner. Through transcriptional downregulation of SQLE, p53 represses cholesterol production in vivo and in vitro, leading to tumor growth suppression. Inhibition of SQLE using small interfering RNA (siRNA) or terbinafine (a SQLE inhibitor) reverses the increased cell proliferation caused by p53 deficiency. Conversely, SQLE overexpression or cholesterol addition promotes cell proliferation, particularly in p53 wild-type cells. More importantly, pharmacological inhibition or shRNA-mediated silencing of SQLE restricts nonalcoholic fatty liver disease (NAFLD)-induced liver tumorigenesis in p53 knockout mice. Therefore, our findings reveal a role for p53 in regulating SQLE and cholesterol biosynthesis, and further demonstrate that downregulation of SQLE is critical for p53-mediated tumor suppression.
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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.