ArticleJournal of clinical and experimental hematopathology : JCEH2022
Cholesterol metabolism and lipid droplet vacuoles; a potential target for the therapy of aggressive lymphoma.
Article in Journal of clinical and experimental hematopathology : JCEH, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Subtype-specific mechanisms of lipid metabolism in gynecological malignancies and novel targeted intervention strategies (Review).Oncology letters · 2026Review
- Scavenger receptor class B type I (SR-BI) as a potential therapeutic target in multiple myeloma.Medical molecular morphology · 2026Article
- Lipid Droplets in Cancer: New Insights and Therapeutic Potential.International journal of molecular sciences · 2026Review
- Scrutinized lipid utilization disrupts Amphotericin-B responsiveness in clinical isolates ofeLife · 2025Article
- Article
- Emergence of Lipid Droplets in the Mechanisms of Carcinogenesis and Therapeutic Responses.Cancers · 2023Review
- Orchestral role of lipid metabolic reprogramming in T-cell malignancy.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
Cholesterol uptake via LDL receptor (LDLR) is increased in some malignant tumors, and incorporated LDL contribute to lipid droplet formation. Burkitt's lymphoma is known to have a large number of vacuoles in the cytoplasm, however, intracellular vacuoles are also seen in high-grade lymphomas such as adult T-cell leukemia/lymphoma, diffuse large B-cell lymphoma and primary central nervous system lymphoma. Recent studies have shown that esterified cholesterol is the main component of these vacuoles and the expression of cholesterol metabolism-related molecules such as LDLR, acetyl-CoA acetyltransferase 1 (ACAT1) which esterifies free cholesterol, and scavenger receptor class B type I (SR-BI) which effluxes free cholesterol, was significantly upregulated in lymphoma cells. Moreover, negative feedback of LDLR was not regulated even under cholesterol-rich conditions in lymphoma cells. We found that cytoplasmic free cholesterol was increased by ACAT and SR-BI inhibitors (CI-976 and BLT-1, respectively), and the accumulation of free cholesterol induced lymphoma cell apoptosis. In addition, overexpression of lipid droplet surface proteins has been correlated with poor prognosis in several malignant tumor such as ovarian cancer and clear cell renal cell carcinoma, and it is important to evaluate lipid droplet formation in malignant tumors including lymphomas.
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