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March 2, 2015Molecular Cancer ResearchOpen Access

Aberrant LPL Expression, Driven by STAT3, Mediates Free Fatty Acid Metabolism in CLL Cells

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Key result

Inhibition of STAT3 or LPL in chronic lymphocytic leukemia cells decreased their capacity to oxidize free fatty acids and reduced cell viability.

Population

Chronic lymphocytic leukemia (CLL) cells, normal B cells, and MM1 cells

Design

Preclinical

Authors

URUri RozovskiRabin Medical CenterSGSrđana GrgurevićCBCarlos Bueso-RamosThe University of Texas MD Anderson Cancer Center

Discussion

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Implication

STAT3-LPL inhibition impairs CLL metabolism in models; leaves open whether this axis is a viable therapeutic target in patients.

Structured PICO

P
Population
Chronic lymphocytic leukemia (CLL) cells, normal B cells, and MM1 cells
I
Intervention
Transfection with STAT3-shRNA or LPL-siRNAs
O
Outcome
Capacity to oxidize free fatty acids (FFAs) and cell viabilitysurrogate

STAT3 induces LPL expression in CLL cells, enabling them to oxidize free fatty acids, suggesting STAT3 inhibition could target CLL cell metabolism.

Cite This Study

Rozovski et al. (2015) studied Chronic lymphocytic leukemia (CLL). STAT3 and LPL inhibition (STAT3-shRNA, LPL-siRNAs) was evaluated on LPL expression, free fatty acid oxidation capacity, and cell viability. Inhibition of STAT3 or LPL in chronic lymphocytic leukemia cells decreased their capacity to oxidize free fatty acids and reduced cell viability.

synapsesocial.com/papers/6ab330e63742ac5ca3067ebehttps://doi.org/10.1158/1541-7786.mcr-14-0412
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Also Consider

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  1. 1A Road Map for Those Who Don't Know JAK-STAT2002 · 1,355 citations
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