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STAT3 Stabilizes C/EBPβ in H-Ras Transformed Mammary Epithelial Cells
인체유방상피세포에서 STAT3에의한 C/EBPβ 안정화

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Authors
이릴리
Advisor
서영준
Major
약학대학 약학과
Issue Date
2015-02
Publisher
서울대학교 대학원
Keywords
STAT3C/EBPβCancer-associated inflammationH-Ras MCF10A
Description
학위논문 (석사)-- 서울대학교 대학원 : 약학과, 2015. 2. 서영준.
Abstract
STAT3 (Signal transducer and activator of transcription 3) plays important roles in cancer-related inflammation by controlling expression of pro-inflammatory cytokines and chemokines. Recent studies suggest STAT3 and C/EBPβ (CCAAT-enhancer binding protein beta) synergistically increase cancer cell proliferation and epithelial-mesenchyml transition (EMT) in breast and brain cancer respectively. C/EBPβ is a leucine-zipper transcription factor that regulates expression of a variety of inflammatory cytokines or chemokines, such as IL-8, G-CSF (granulocyte colony stimulating factor), and GM-CSF (granulocyte macrophage colony stimulating factor) which induce neutrophil infiltration and differentiation. However, the molecular mechanism by which STAT3 and C/EBPβ cooperatively interact has not been fully elucidated. In this study, I found that the level of C/EBPβ protein but not that of its mRNA transcript was decreased in the absence of STAT3 in H-Ras MCF10A cells. In addition, silencing STAT3 dramatically induced proteasomal degradation of C/EBPβ and thus suppressed transcription of C/EBPβ target genes. Furthermore, direct interaction between STAT3 and C/EBPβ was confirmed by immuno-precipitation. Taken together, STAT3 stabilizes C/EBPβ thereby promoting cancer-associated inflammation.
Language
English
URI
https://hdl.handle.net/10371/133577
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College of Pharmacy (약학대학)Dept. of Pharmacy (약학과)Theses (Master's Degree_약학과)
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