ArticleMolecular cancer research : MCR2015
Aberrant LPL Expression, Driven by STAT3, Mediates Free Fatty Acid Metabolism in CLL Cells.
Article in Molecular cancer research : MCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 89 citations in OpenAlex.
- The Critical Role of Adipocytes in Leukemia.Biology · 2025Review
- Complementary approaches define the metabolic features that accompany Richter syndrome transformation.Cellular and molecular life sciences : CMLS · 2025Article
- Fatty acid metabolism shapes immune responses in chronic lymphocytic leukemia.Biomarker research · 2025Article
- CAMKIIδ Reinforces Lipid Metabolism and Promotes the Development of B Cell Lymphoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- ENPP2 promotes progression and lipid accumulation via AMPK/SREBP1/FAS pathway in chronic lymphocytic leukemia.Cellular & molecular biology letters · 2024Article
- Leveraging altered lipid metabolism in treating B cell malignancies.Progress in lipid research · 2024Review
- Non-canonical transcriptional regulation of the poor prognostic factor UGT2B17 in chronic lymphocytic leukemic and normal B cells.BMC cancer · 2024Article
- Investigation of fatty acid metabolism in chronic lymphocytic leukemia to guide clinical outcome and therapy.Annals of hematology · 2024Article
- ACOX1-mediated peroxisomal fatty acid oxidation contributes to metabolic reprogramming and survival in chronic lymphocytic leukemia.Leukemia · 2024Article
- Triptolide Reduces Neoplastic Progression in Hepatocellular Carcinoma by Downregulating the Lipid Lipase Signaling Pathway.Cancers · 2024Article
- m6A-Modified circTET2 Interacting with HNRNPC Regulates Fatty Acid Oxidation to Promote the Proliferation of Chronic Lymphocytic Leukemia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The Role of Cholesterol in Chronic Lymphocytic Leukemia Development and Pathogenesis.Metabolites · 2023Review
- Proteomic and phosphoproteomic analysis reveal threonine deficiency increases hepatic lipid deposition in Pekin ducks via reducing STAT phosphorylation.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2023Article
- Ameliorating effect of probiotic on nonalcoholic fatty liver disease and lipolytic gene expression in rabbits.Scientific reports · 2023Article
- Review
- STAT proteins in cancer: orchestration of metabolism.Nature reviews. Cancer · 2023Review
- Metabolomics: A New Era in the Diagnosis or Prognosis of B-Cell Non-Hodgkin's Lymphoma.Diagnostics (Basel, Switzerland) · 2023Review
- Current Status of Novel Agents for the Treatment of B Cell Malignancies: What's Coming Next?Cancers · 2022Review
- Targeting metabolic reprogramming in chronic lymphocytic leukemia.Experimental hematology & oncology · 2022Review
- Regulation of S100As Expression by Inflammatory Cytokines in Chronic Lymphocytic Leukemia.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledWhile reviewing chronic lymphocytic leukemia (CLL) bone marrow slides, we identified cytoplasmic lipid vacuoles in CLL cells but not in normal B cells. Because lipoprotein lipase (LPL), which catalyzes hydrolysis of triglycerides into free fatty acids (FFA), is aberrantly expressed in CLL, we investigated whether LPL regulates the oxidative metabolic capacity of CLL cells. We found that unlike normal B cells, CLL cells metabolize FFAs. Because STAT3 is constitutively activated in CLL cells and because we identified putative STAT3 binding sites in the LPL promoter, we sought to determine whether STAT3 drives the aberrant expression of LPL. Transfection of luciferase reporter gene constructs driven by LPL promoter fragments into MM1 cells revealed that STAT3 activates the LPL promoter. In addition, chromatin immunoprecipitation confirmed that STAT3 binds to the LPL promoter. Furthermore, transfection of CLL cells with STAT3-shRNA downregulated LPL transcripts and protein levels, confirming that STAT3 activates the LPL gene. Finally, transfection of CLL cells with LPL-siRNAs decreased the capacity of CLL cells to oxidize FFAs and reduced cell viability. IMPLICATIONS: Our study suggests that CLL cells adopt their metabolism to oxidize FFA. Activated STAT3 induces LPL, which catalyzes the hydrolysis of triglycerides into FFA. Therefore, inhibition of STAT3 is likely to prevent the capacity of CLL cells to utilize FFA.
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