ArticleCell reports2015
Hepatic SirT1-Dependent Gain of Function of Stearoyl-CoA Desaturase-1 Conveys Dysmetabolic and Tumor Progression Functions.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- A stearate-rich diet and oleate restriction directly inhibit tumor growth via the unfolded protein response.Experimental & molecular medicine · 2024Article
- Preclinical Evaluation of NTX-301, a Novel DNA Hypomethylating Agent in Ovarian Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Unveiling the MUFA-Cancer Connection: Insights from Endogenous and Exogenous Perspectives.International journal of molecular sciences · 2023Review
- C-Terminal Truncated HBx Facilitates Oncogenesis by Modulating Cell Cycle and Glucose Metabolism in FXR-Deficient Hepatocellular Carcinoma.International journal of molecular sciences · 2023Article
- Ptpn1 deletion protects oval cells against lipoapoptosis by favoring lipid droplet formation and dynamics.Cell death and differentiation · 2022Article
- Wnt/β-Catenin Signaling as a Driver of Stemness and Metabolic Reprogramming in Hepatocellular Carcinoma.Cancers · 2022Review
- Analysis of rare genetic variation underlying cardiometabolic diseases and traits among 200,000 individuals in the UK Biobank.Nature genetics · 2022Article
- Metabolic dysregulation and emerging therapeutical targets for hepatocellular carcinoma.Acta pharmaceutica Sinica. B · 2022Review
- Voluntary exercise training improves body weight of leptin-deficient ob/ob mice by altering hepatic stearoyl-CoA desaturase 1 and deleted in breast cancer 1 protein levels.Physical activity and nutrition · 2021Article
- Modulation of SCD1 activity in hepatocyte cell lines: evaluation of genomic stability and proliferation.Molecular and cellular biochemistry · 2021Article
- CCAR1 and CCAR2 as gene chameleons with antagonistic duality: Preclinical, human translational, and mechanistic basis.Cancer science · 2020Review
- Lung fibroblasts promote metastatic colonization through upregulation of stearoyl-CoA desaturase 1 in tumor cells.Oncogene · 2018Article
- Inhibition of Mdmx (Mdm4)Oncotarget · 2018Article
- Haploinsufficiency of SIRT1 Enhances Glutamine Metabolism and Promotes Cancer Development.Current biology : CB · 2017Article
- Fatty Acids and Breast Cancer: Make Them on Site or Have Them Delivered.Journal of cellular physiology · 2016Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Obesity is associated with higher incidence of cancer, but the predisposing mechanisms remain poorly understood. The NAD(+)-dependent deacetylase SirT1 orchestrates metabolism, cellular survival, and growth. However, there is no unifying mechanism to explain the metabolic and tumor-related effects of SirT1. In this work, we demonstrate that genetic ablation of the endogenous inhibitor of SirT1, Deleted-in-Breast-Cancer-1 (Dbc1), unexpectedly results in obesity and insulin resistance. Dbc1 deficiency promoted SirT1-dependent gain of function of stearoyl-coenzyme A desaturase 1 (Scd1), increasing plasma and tissue levels of unsaturated fatty acids. The metabolic abnormalities in Dbc1(-/-) mice were reversed by ablation of hepatic SirT1 or by inhibition of Scd1 activity. Furthermore, loss of Dbc1 impaired activation of the master tumor suppressor p53 and treatment with an Scd1 inhibitor extended survival of tumor-prone TP53(-/-) mice by decreasing tumor-related death. Together, our findings illustrate a shared mechanism of obesity and tumor progression mediated by hepatic SirT1 and resulting in the activation of a key lipid synthetic enzyme, with potential therapeutic implications.
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