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Selenium regulates cyclooxygenase-2 and extracellular signal-regulated kinase signaling pathways by activating AMP-activated protein kinase in colon cancer cells
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Hwang, Jin-Taek | - |
dc.contributor.author | Kim, Young Min | - |
dc.contributor.author | Surh, Young-Joon | - |
dc.contributor.author | Baik, Haing Woon | - |
dc.contributor.author | Lee, Seong Yu | - |
dc.contributor.author | Ha, Joohun | - |
dc.contributor.author | Park, Ock Jin | - |
dc.date.accessioned | 2021-01-31T10:14:38Z | - |
dc.date.available | 2021-01-31T10:14:38Z | - |
dc.date.created | 2017-11-15 | - |
dc.date.issued | 2006-10 | - |
dc.identifier.citation | Cancer Research, Vol.66 No.20, pp.10057-10063 | - |
dc.identifier.issn | 0008-5472 | - |
dc.identifier.other | 3626 | - |
dc.identifier.uri | https://hdl.handle.net/10371/172753 | - |
dc.description.abstract | Epidemiologic and experimental evidences indicate that selenium, an essential trace element, can reduce the risk of a variety of cancers. Protection against certain types of cancers, particularly colorectal cancers, is closely associated with Pathways involving cyclooxygenase-2 (COX-2). We found that AMP-activated protein kinase (AMPK), which functions as a cellular energy sensor, mediates critical anticancer effects of selenium via a COX-2/prostaglandin E-2 signaling pathway. Selenium activated AMPK in tumor xenografts as well as in colon cancer cell lines, and this activation seemed to he essential to the decrease in COX-2 expressions. Transduction with dominant-negative AMPK into colon cancer cells or application of cox-2(-/-)-negative cells supported the evidence that AMPK is an upstream signal of COX-2 and inhibits cell proliferation. In HT-29 colon cancer cells, carcinogenic agent 12-O-tetradecanoylphorbol-13-acetate (TPA) activated extracellular signal-regulated kinase (ERK) that led to COX-2 expression and selenium blocked the TPA-induced ERK and COX-2 activation via AMPK. We also showed the role of a reactive oxygen species as an AMPK activation signal in selenium-treated cells. We propose that AMPK is a novel and critical regulatory component in selenium-induced cancer cell death, further implying AMPK as a prime target of tumorigenesis. | - |
dc.language | 영어 | - |
dc.publisher | American Association for Cancer Research | - |
dc.title | Selenium regulates cyclooxygenase-2 and extracellular signal-regulated kinase signaling pathways by activating AMP-activated protein kinase in colon cancer cells | - |
dc.type | Article | - |
dc.contributor.AlternativeAuthor | 서영준 | - |
dc.identifier.doi | 10.1158/0008-5472.CAN-06-1814 | - |
dc.citation.journaltitle | Cancer Research | - |
dc.identifier.wosid | 000241392700034 | - |
dc.identifier.scopusid | 2-s2.0-33750535008 | - |
dc.citation.endpage | 10063 | - |
dc.citation.number | 20 | - |
dc.citation.startpage | 10057 | - |
dc.citation.volume | 66 | - |
dc.identifier.sci | 000241392700034 | - |
dc.description.isOpenAccess | N | - |
dc.contributor.affiliatedAuthor | Surh, Young-Joon | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | COLORECTAL-CANCER | - |
dc.subject.keywordPlus | DU145 CELLS | - |
dc.subject.keywordPlus | GROWTH | - |
dc.subject.keywordPlus | COX-2 | - |
dc.subject.keywordPlus | CHEMOPREVENTION | - |
dc.subject.keywordPlus | LKB1 | - |
dc.subject.keywordPlus | INHIBITION | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | GENISTEIN | - |
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