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N-hydroxy-7-(2-naphthylthio) heptanomide (HNHA), histone deacetylase inhibitors, suppresses COX-2 expression in colon cancer
DC Field | Value | Language |
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dc.contributor.author | 박지현 | - |
dc.date.accessioned | 2015-11-21T07:40:55Z | - |
dc.date.available | 2015-11-21T07:40:55Z | - |
dc.date.issued | 2009 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/124893 | - |
dc.description | Dept. of Medical Science/석사 | - |
dc.description.abstract | [한글] [영문] Cyclooxygenase-2 (COX-2) plays important roles in cell adhesion, apoptosis, and angiogenesis, and is essential for tumor angiogenesis. Levels of COX-2 expression are low in normal cells, but very high level in human and animal colorectal tumors.Histone deacetylase (HDAC) plays a crucial role in carcinogenesis1 and is over-expressed in several tumor cells2. The histone deacetylase inhibitor N-hydroxy-7-(2-naphthylthio) heptanomide (HNHA) is a new anti-angiogenesis drug, and has been shown to inhibit COX-2 expression in colon cancer. Here, we confirm that HNHA decreases COX-2 expression in colon cancer, similar to COX-2 inhibitors such as Celecoxib and Rofecoxib. Moreover, hypoxia inducible factor-1α (HIF-1α), and tumor necrosis factor-α (TNF-α) are involved in COX-2 expression and their expression is also decreased by HNHA in colon cancer. The effect of HNHA on tumor growth was examined in a human colon cancer tumor model and investigated by western blot, immunohistochemistry, and FACS analysis. | - |
dc.description.statementOfResponsibility | open | - |
dc.publisher | Graduate School, Yonsei University | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.title | N-hydroxy-7-(2-naphthylthio) heptanomide (HNHA), histone deacetylase inhibitors, suppresses COX-2 expression in colon cancer | - |
dc.title.alternative | 대장암에서 신약 HNHA (N-hydroxy-7-(2-naphthylthio) heptanomide) 의 COX-2 | - |
dc.type | Thesis | - |
dc.contributor.alternativeName | Park, Ji Hyun | - |
dc.type.local | Thesis | - |
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