Publications
Detailed Information
Sunitinib deregulates tumor adaptation to hypoxia by inhibiting HIF-1α synthesis in HT-29 colon cancer cells
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Shin, Hyun-Woo | - |
dc.contributor.author | Cho, Chung-Hyun | - |
dc.contributor.author | Kim, Tae-You | - |
dc.contributor.author | Park, Jong-Wan | - |
dc.date.accessioned | 2012-05-25T06:36:31Z | - |
dc.date.available | 2012-05-25T06:36:31Z | - |
dc.date.issued | 2010-07-23 | - |
dc.identifier.citation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS; Vol.398 2; 205-211 | ko_KR |
dc.identifier.issn | 0006-291X | - |
dc.identifier.uri | https://hdl.handle.net/10371/76478 | - |
dc.description.abstract | Sunitinib (SU11248, Sutent (R)) is a class III/V receptor tyrosine kinase (RTK) inhibitor that exhibits potent anti-angiogenic and anticancer activities. Preclinical studies demonstrated that the sunitinib effects are attributed to inhibition of VEGFR and PDGFR phosphorylation. However, even in colon cancer cells lacking sunitinib-targeted RTKs, sunitinib effectively inhibits tumor growth in a xenograft model, and this raises a question about the mechanism underlying the in vivo anticancer action of sunitinib. Since hypoxia is a critical microenvironment that tumors face, we addressed the possibility that sunitinib deregulates tumor adaptation to hypoxia. First we found that sunitinib limits the colony growth of HT-29, which is a colon adenocarcinoma cell line lacking the RTKs, and that HIF-1 alpha in the colonies is decreased by sunitinib. In cultured HT-29 cells, sunitinib suppressed HIF-1 alpha under hypoxic conditions. Moreover, sunitinib repressed the activity of HIF-1 alpha and subsequently decreased the expressions of HIF-1 downstream genes. Mechanistically, sunitinib blocked the 5`-UTR-dependent translation of HIF-1 alpha. The HIF-1 alpha suppression by sunitinib was also reproduced in a VHL-null renal cell carcinoma cell line, where HIF-1 alpha is not degradable. In conclusion, the sunitinib inhibition of HIF-1 signaling could restrain tumor progression in hypoxic regions, which may contribute to anticancer effect of sunitinib. (C) 2010 Elsevier Inc. All rights reserved. | ko_KR |
dc.language.iso | en | ko_KR |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | ko_KR |
dc.subject | Sunitinib | ko_KR |
dc.subject | Tumor hypoxia | ko_KR |
dc.subject | Colony formation | ko_KR |
dc.subject | Protein synthesis | ko_KR |
dc.subject | Hypoxia-inducible factor 1 | ko_KR |
dc.title | Sunitinib deregulates tumor adaptation to hypoxia by inhibiting HIF-1α synthesis in HT-29 colon cancer cells | ko_KR |
dc.type | Article | ko_KR |
dc.contributor.AlternativeAuthor | 신현우 | - |
dc.contributor.AlternativeAuthor | 조정현 | - |
dc.contributor.AlternativeAuthor | 김태유 | - |
dc.contributor.AlternativeAuthor | 박종완 | - |
dc.identifier.doi | 10.1016/j.bbrc.2010.06.060 | - |
dc.citation.journaltitle | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.description.citedreference | Sonpavde G, 2009, UROL ONCOL-SEMIN ORI, V27, P391, DOI 10.1016/j.urolonc.2008.03.017 | - |
dc.description.citedreference | Kontovinis LF, 2009, BMC CANCER, V9, DOI 10.1186/1471-2407-9-82 | - |
dc.description.citedreference | CHO YS, 2009, MOL CELLS | - |
dc.description.citedreference | BURKITT K, 2009, MOL CANC THER | - |
dc.description.citedreference | Birk DM, 2008, VASC ENDOVASC SURG, V42, P517, DOI 10.1177/1538574408322755 | - |
dc.description.citedreference | Rini BI, 2008, J CLIN ONCOL, V26, P3743, DOI 10.1200/JCO.2007.15.5416 | - |
dc.description.citedreference | Chow LQM, 2007, J CLIN ONCOL, V25, P884, DOI 10.1200/JCO.2006.06.3602 | - |
dc.description.citedreference | Motzer RJ, 2007, NEW ENGL J MED, V356, P115 | - |
dc.description.citedreference | Patel PH, 2006, CLIN CANCER RES, V12, P7215, DOI 10.1158/1078-0432.CCR-06-2254 | - |
dc.description.citedreference | Demetri GD, 2006, LANCET, V368, P1329, DOI 10.1016/S0140-6736(06)69446-4 | - |
dc.description.citedreference | Potapova O, 2006, MOL CANCER THER, V5, P1280, DOI 10.1158/1535-7163.MCT-03-0156 | - |
dc.description.citedreference | Yeo EJ, 2006, BLOOD, V107, P916, DOI 10.1182/blood-2005-06-2564 | - |
dc.description.citedreference | Chen WT, 2005, JPN J CLIN ONCOL, V35, P207, DOI 10.1093/jjco/hyi067 | - |
dc.description.citedreference | GINGERICH TJ, 2004, ANIM HEALTH RES REV, V5, P49, DOI 10.1079/AHRR200460 | - |
dc.description.citedreference | Takahashi R, 2003, ONCOL REP, V10, P797 | - |
dc.description.citedreference | Yeo EJ, 2003, J NATL CANCER I, V95, P516 | - |
dc.description.citedreference | Mendel DB, 2003, CLIN CANCER RES, V9, P327 | - |
dc.description.citedreference | Hudson CC, 2002, MOL CELL BIOL, V22, P7004, DOI 10.1128/MCB.22.20.7004-7014.2002 | - |
dc.description.citedreference | Lang KJD, 2002, MOL BIOL CELL, V13, P1792, DOI 10.1091/mbc.02-02-0017 | - |
dc.description.citedreference | Arsham AM, 2002, J BIOL CHEM, V277, P15162, DOI 10.1074/jbc.M111162200 | - |
dc.description.citedreference | Laughner E, 2001, MOL CELL BIOL, V21, P3995 | - |
dc.description.citedreference | Yamashita K, 2001, J BIOL CHEM, V276, P12645 | - |
dc.description.citedreference | Hockel M, 2001, J NATL CANCER I, V93, P266 | - |
dc.description.citedreference | Tanimoto K, 2000, EMBO J, V19, P4298 | - |
dc.description.citedreference | Talks KL, 2000, AM J PATHOL, V157, P411 | - |
dc.description.citedreference | Chun YS, 2000, BIOCHEM BIOPH RES CO, V268, P652 | - |
dc.description.citedreference | TAKAHASHI Y, 1995, CANCER RES, V55, P3964 | - |
dc.description.citedreference | WANG GL, 1995, P NATL ACAD SCI USA, V92, P5510 | - |
dc.description.tc | 4 | - |
- Appears in Collections:
- Files in This Item:
- There are no files associated with this item.
Item View & Download Count
Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.