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Induction of DNA Damage-Inducible Gene GADD45β Contributes to Sorafenib-Induced Apoptosis in Hepatocellular Carcinoma Cells
Cancer research (Chicago, Ill.), 2010-11, Vol.70 (22), p.9309-9318
OU, Da-Liang
SHEN, Ying-Chun
CHENG, Ann-Lii
YU, Sung-Liang
CHEN, Kuen-Feng
YEH, Pei-Yen
FAN, Hsiang-Hsuan
FENG, Wen-Chi
WANG, Ching-Tzu
LIN, Liang-In
HSU, Chiun
2010
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Autor(en) / Beteiligte
OU, Da-Liang
SHEN, Ying-Chun
CHENG, Ann-Lii
YU, Sung-Liang
CHEN, Kuen-Feng
YEH, Pei-Yen
FAN, Hsiang-Hsuan
FENG, Wen-Chi
WANG, Ching-Tzu
LIN, Liang-In
HSU, Chiun
Titel
Induction of DNA Damage-Inducible Gene GADD45β Contributes to Sorafenib-Induced Apoptosis in Hepatocellular Carcinoma Cells
Ist Teil von
Cancer research (Chicago, Ill.), 2010-11, Vol.70 (22), p.9309-9318
Ort / Verlag
Philadelphia, PA: American Association for Cancer Research
Erscheinungsjahr
2010
Quelle
EZB Electronic Journals Library
Beschreibungen/Notizen
Abstract Markers that could accurately predict responses to the general kinase inhibitor sorafenib are needed to better leverage its clinical applications. In this study, we examined a hypothesized role in the drug response for the growth arrest DNA damage-inducible gene 45β (GADD45β), which is commonly underexpressed in hepatocellular carcinoma (HCC) where sorafenib may offer an important new therapeutic option. The anticancer activity of sorafenib-induced GADD45β expression was tested in a panel of HCC cell lines and xenograft models. We found that GADD45β mRNA and protein expression were induced relatively more prominently in HCC cells that were biologically sensitive to sorafenib treatment. GADD45β induction was not found after treatment with either the mitogen-activated protein kinase–extracellular signal-regulated kinase (ERK) kinase (MEK) inhibitor U0126 or the Raf inhibitor ZM336372, suggesting that GADD45β induction by sorafenib was independent of Raf/MEK/ERK signaling activity. However, c-Jun NH2-terminal kinase (JNK) kinase activation occurred preferentially in sorafenib-sensitive cells. Small interfering RNA–mediated knockdown of GADD45βor JNK kinase limited the proapoptotic effects of sorafenib in sorafenib-sensitive cells. We defined the −339/−267 region in the GADD45β promoter containing activator protein-1 and SP1-binding sites as a crucial region for GADD45β induction by sorafenib. Together, our findings suggest that GADD45β induction contributes to sorafenib-induced apoptosis in HCC cells, prompting further studies to validate its potential value in predicting sorafenib efficacy. Cancer Res; 70(22); 9309–18. ©2010 AACR.
Sprache
Englisch
Identifikatoren
ISSN: 0008-5472
eISSN: 1538-7445
DOI: 10.1158/0008-5472.CAN-10-1033
Titel-ID: cdi_proquest_miscellaneous_856775417
Format
–
Schlagworte
Antineoplastic agents
,
Biological and medical sciences
,
Gastroenterology. Liver. Pancreas. Abdomen
,
Liver. Biliary tract. Portal circulation. Exocrine pancreas
,
Medical sciences
,
Pharmacology. Drug treatments
,
Tumors
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