ArticleOncogenesis2018
Fatostatin induces pro- and anti-apoptotic lipid accumulation in breast cancer.
Article in Oncogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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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.
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
40 citing papers in PubMed, 61 citations in OpenAlex.
- Sterol regulatory element‑binding proteins: Master regulators of lipid metabolic reprogramming in cancer and emerging therapeutic targets (Review).Oncology reports · 2026Review
- SREBP2 regulates CCDC25 expression and promotes tumor metastasis in Triple-Negative Breast Cancer.Oncogenesis · 2026Article
- Evaluation of selected indigenous spices- and herbs-derived small molecules as potential inhibitors of SREBP and its implications for breast cancer using MD simulations and MMPBSA calculations.Molecular diversity · 2025Article
- Ferroptosis as a therapeutic target in glioblastoma: Mechanisms and emerging strategies.Molecular therapy. Nucleic acids · 2025Review
- Fatostatin delayed lip sensory recovery after inferior alveolar nerve transection by inhibiting sterol regulatory element-binding protein 1.Journal of dental sciences · 2025Article
- SREBP-1 in obesity-induced breast cancer: mechanisms and therapeutic perspectives.Molecular biology reports · 2025Review
- Understanding the Link Between Sterol Regulatory Element Binding Protein (SREBPs) and Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD).Current obesity reports · 2025Review
- Lipid metabolic reprograming: the unsung hero in breast cancer progression and tumor microenvironment.Molecular cancer · 2025Review
- Inhibition of STRA6 suppresses NSCLC growth via blocking STAT3/SREBP-1c axis-mediated lipogenesis.Molecular and cellular biochemistry · 2025Article
- Crosstalk between lipid metabolism and EMT: emerging mechanisms and cancer therapy.Molecular and cellular biochemistry · 2025Article
- The SARIFA biomarker in the context of basic research of lipid-driven cancers.NPJ precision oncology · 2024Review
- Unraveling the intricate relationship between lipid metabolism and oncogenic signaling pathways.Frontiers in cell and developmental biology · 2024Review
- Review
- Fatostatin induces ferroptosis through inhibition of the AKT/mTORC1/GPX4 signaling pathway in glioblastoma.Cell death & disease · 2023Article
- Key events in cancer: Dysregulation of SREBPs.Frontiers in pharmacology · 2023Review
- Emerging Roles of Ceramides in Breast Cancer Biology and Therapy.International journal of molecular sciences · 2022Review
- Posttranslational control of lipogenesis in the tumor microenvironment.Journal of hematology & oncology · 2022Review
- Impact of Tralopyril and Triazolyl Glycosylated Chalcone in Human Retinal Cells' Lipidome.Molecules (Basel, Switzerland) · 2022Article
- Lipid Metabolism in Glioblastoma: From De Novo Synthesis to Storage.Biomedicines · 2022Review
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Given the dependence of cancers on de novo lipogenesis, we tested the effect of fatostatin, a small molecule thought to target this pathway by blocking activation of SREBP transcription factors, in breast cancer cell lines and xenograft tumors. We found that estrogen receptor (ER) positive cells were more sensitive to fatostatin than ER negative cells and responded with cell cycle arrest and apoptosis. Surprisingly, we found that rather than inhibiting lipogenesis, fatostatin caused an accumulation of lipids as a response to endoplasmic reticulum stress rather than inhibition of SREBP activity. In particular, ceramide and dihydroceramide levels increased and contributed to the apoptotic effects of fatostatin. In addition, an accumulation of triacylglycerides (TAGs), particularly those containing polyunsaturated fatty acids (PUFAs), was also observed as a result of elevated diacylglycerol transferase activity. Blocking PUFA-TAG production enhanced the apoptotic effect of fatostatin, suggesting that these lipids play a protective role and limit fatostatin response. Together, these findings indicate that the ability of breast cancer cells to respond to fatostatin depends on induction of endoplasmic reticulum stress and subsequent ceramide accumulation, and that limiting production of PUFA-TAGs may be therapeutically beneficial in specific tumor subtypes.
Identifiers
What OpenQuestion holds
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.