Abstract
We previously demonstrated that the brain, pituitary, and C6 glioblastoma cells express leptin. To determine the physiological role of brain-derived leptin, we sought to selectively silence its expression using RNA interference (RNAi) in vitro. One of four potential targets, siRNA L7, reduced leptin mRNA by 50% (P < 0.05) and protein by 55% (P < 0.0001) in C6 cells. RNAi also induced a twofold increase in cell death as seen by ethidium homodimer-1 (P < 0.015) and TUNEL (P < 0.005) staining. These data suggest that endogenous leptin may be a critical factor promoting cell survival in the brain.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Analysis of Variance
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Animals
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Cell Count
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Cell Death / drug effects
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Cell Line, Tumor
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Dose-Response Relationship, Drug
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Gene Expression Regulation / drug effects*
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Gene Silencing / drug effects*
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Glioblastoma / pathology
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Glioblastoma / physiopathology
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Leptin / genetics
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Leptin / metabolism*
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RNA Interference
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RNA, Messenger / biosynthesis
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RNA, Neoplasm / genetics
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RNA, Neoplasm / metabolism
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RNA, Small Interfering / pharmacology*
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Rats
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Reverse Transcriptase Polymerase Chain Reaction
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Ribosomal Proteins / physiology
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Time Factors
Substances
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Leptin
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RNA, Messenger
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RNA, Neoplasm
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RNA, Small Interfering
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Ribosomal Proteins