ArticleJournal of lipid research2016
Fatostatin blocks ER exit of SCAP but inhibits cell growth in a SCAP-independent manner.
Article in Journal of lipid research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
59 citing papers in PubMed, 76 citations in OpenAlex.
- An oral nanocombinatorial agent exhibits pleiotropic improvement in diabetic nephropathy via modulation of the SCAP/SREBPs pathway.Journal of nanobiotechnology · 2026Article
- Mechanism-based new approach methodologies for in vitro detection of chemical-induced liver steatosis.Archives of toxicology · 2026Review
- Serum lipidome remodeling in viral pneumonia: from pathophysiology to therapeutics.Frontiers in immunology · 2026Review
- ARL5B Drives Esophageal Squamous Cell Carcinoma Progression via ROCK1-SREBP1-Mediated Lipid Metabolic Reprogramming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Discovery of highly potent marine-derived compound Penicolinate H reveals SREBP-1 mediated lipogenesis as a druggable vulnerability in gastric cancer.Journal of translational medicine · 2025Article
- Reprogrammed Lipid Metabolism-Associated Therapeutic Vulnerabilities in Prostate Cancer.International journal of molecular sciences · 2025Review
- Structural basis for substrate selectivity by site-one protease revealed by studies with a small-molecule inhibitor.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Targeting oncogenic activation of FLT3/SREBP/FASN promotes the therapeutic effect of quizartinib involving disruption of mitochondrial phospholipids.Cell death & disease · 2025Article
- Understanding the Link Between Sterol Regulatory Element Binding Protein (SREBPs) and Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD).Current obesity reports · 2025Review
- Lipolysis-derived fatty acids are needed for homeostatic control of sterol element-binding protein-1c driven hepatic lipogenesis.Communications biology · 2025Article
- The Role of Cholesterol Metabolism and Its Regulation in Tumor Development.Cancer medicine · 2025Review
- SREBP2 as a central player in cancer progression: potential for targeted therapeutics.Frontiers in pharmacology · 2025Review
- Advances in Mendelian Randomization Studies of Obesity Over the Past Decade: Uncovering Key Genetic Mechanisms.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- Article
- A High-Throughput Screening Platform Identifies FDA-Approved Drugs That Inhibit SREBP Pathway Activation.ACS chemical biology · 2024Article
- Human cytomegalovirus infection impairs neural differentiation via repressing sterol regulatory element binding protein 2-mediated cholesterol biosynthesis.Cellular and molecular life sciences : CMLS · 2024Article
- Regulation and targeting of SREBP-1 in hepatocellular carcinoma.Cancer metastasis reviews · 2024Review
- A cholesterol-binding bacterial toxin provides a strategy for identifying a specific Scap inhibitor that blocks lipid synthesis in animal cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Unveiling the STAT3-ACC1 axis: a key driver of lipid metabolism and tumor progression in non-small cell lung cancer.Journal of Cancer · 2024Article
- Cholesterol biosynthesis modulates differentiation in murine cranial neural crest cells.Scientific reports · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Sterol regulatory element-binding protein (SREBP) transcription factors are central regulators of cellular lipid homeostasis and activate expression of genes required for fatty acid, triglyceride, and cholesterol synthesis and uptake. SREBP cleavage activating protein (SCAP) plays an essential role in SREBP activation by mediating endoplasmic reticulum (ER)-to-Golgi transport of SREBP. In the Golgi, membrane-bound SREBPs are cleaved sequentially by the site-1 and site-2 proteases. Recent studies have shown a requirement for the SREBP pathway in the development of fatty liver disease and tumor growth, making SCAP a target for drug development. Fatostatin is a chemical inhibitor of the SREBP pathway that directly binds SCAP and blocks its ER-to-Golgi transport. In this study, we determined that fatostatin blocks ER exit of SCAP and showed that inhibition is independent of insulin-induced gene proteins, which function to retain the SCAP-SREBP complex in the ER. Fatostatin potently inhibited cell growth, but unexpectedly exogenous lipids failed to rescue proliferation of fatostatin-treated cells. Furthermore, fatostatin inhibited growth of cells lacking SCAP Using a vesicular stomatitis virus glycoprotein (VSVG) trafficking assay, we demonstrated that fatostatin delays ER-to-Golgi transport of VSVG. In summary, fatostatin inhibited SREBP activation, but fatostatin additionally inhibited cell proliferation through both lipid-independent and SCAP-independent mechanisms, possibly by general inhibition of ER-to-Golgi transport.
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Registered trials
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.