17[beta]-Estradiol inhibits prostaglandin E2-induced COX-2 expressions and cell migration by suppressing Akt and ERK1/2 signaling pathways in human LoVo colon cancer cells
Epidemiological studies demonstrate that the incidence and mortality rates of colorectal cancer in women are lower than in men. However, it is unknown if 17[beta]-estradiol treatment is sufficient to inhibit prostaglandin E2 (PGE2)-induced cellular motility in human colon cancer cells. Upregulation...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2010-09, Vol.342 (1-2), p.63 |
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| creator | Lai, Tung-Yuan Chen, Li-Mien Lin, Jing-Ying Tzang, Bor-Show Lin, James A Tsai, Chang-Hai Lin, Yueh-Min Huang, Chih-Yang Liu, Chung-Jung Hsu, Hsi-Hsien |
| description | Epidemiological studies demonstrate that the incidence and mortality rates of colorectal cancer in women are lower than in men. However, it is unknown if 17[beta]-estradiol treatment is sufficient to inhibit prostaglandin E2 (PGE2)-induced cellular motility in human colon cancer cells. Upregulation of cyclooxygenase-2 (COX-2) is reported to associate with the development of cancer cell mobility, metastasis, and subsequent malignant tumor. After administration of inhibitors including LY294002 (Akt activation inhibitor), U0126 (ERK1/2 inhibitor), SB203580 (p38 MAPK inhibitor), SP600125 (JNK1/2 inhibitor), or QNZ (NF[kappa]B inhibitor), we found that PGE2 treatment increases COX-2 via Akt and ERK1/2 pathways, thus promoting cellular motility in human LoVo cancer cells. We further observed that 17[beta]-estradiol treatment inhibits PGE2-induced COX-2 expression and cellular motility via suppressing activation of Akt and ERK1/2 in human LoVo cancer cells. Collectively, these results suggest that 17[beta]-estradiol treatment dramatically inhibits PGE2-induced progression of human LoVo colon cancer cells. Keywords Estrogen * Prostaglandin E2 * Human colon cancer cell * COX-2 * Cell motility |
| doi_str_mv | 10.1007/s11010-010-0469-7 |
| format | Article |
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However, it is unknown if 17[beta]-estradiol treatment is sufficient to inhibit prostaglandin E2 (PGE2)-induced cellular motility in human colon cancer cells. Upregulation of cyclooxygenase-2 (COX-2) is reported to associate with the development of cancer cell mobility, metastasis, and subsequent malignant tumor. After administration of inhibitors including LY294002 (Akt activation inhibitor), U0126 (ERK1/2 inhibitor), SB203580 (p38 MAPK inhibitor), SP600125 (JNK1/2 inhibitor), or QNZ (NF[kappa]B inhibitor), we found that PGE2 treatment increases COX-2 via Akt and ERK1/2 pathways, thus promoting cellular motility in human LoVo cancer cells. We further observed that 17[beta]-estradiol treatment inhibits PGE2-induced COX-2 expression and cellular motility via suppressing activation of Akt and ERK1/2 in human LoVo cancer cells. Collectively, these results suggest that 17[beta]-estradiol treatment dramatically inhibits PGE2-induced progression of human LoVo colon cancer cells. Keywords Estrogen * Prostaglandin E2 * Human colon cancer cell * COX-2 * Cell motility</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-010-0469-7</identifier><language>eng</language><publisher>New York: Springer</publisher><subject>Biochemistry ; Cancer cells ; Cell adhesion & migration ; Colon cancer ; Colorectal cancer ; Colorectal carcinoma ; COX-2 inhibitors ; Estradiol ; Estrogens ; Gene expression ; Health aspects ; Kinases ; Phenols ; Prostaglandins E ; Signal transduction</subject><ispartof>Molecular and cellular biochemistry, 2010-09, Vol.342 (1-2), p.63</ispartof><rights>COPYRIGHT 2010 Springer</rights><rights>Springer Science+Business Media, LLC. 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Lai, Tung-Yuan</creatorcontrib><creatorcontrib>Chen, Li-Mien</creatorcontrib><creatorcontrib>Lin, Jing-Ying</creatorcontrib><creatorcontrib>Tzang, Bor-Show</creatorcontrib><creatorcontrib>Lin, James A</creatorcontrib><creatorcontrib>Tsai, Chang-Hai</creatorcontrib><creatorcontrib>Lin, Yueh-Min</creatorcontrib><creatorcontrib>Huang, Chih-Yang</creatorcontrib><creatorcontrib>Liu, Chung-Jung</creatorcontrib><creatorcontrib>Hsu, Hsi-Hsien</creatorcontrib><title>17[beta]-Estradiol inhibits prostaglandin E2-induced COX-2 expressions and cell migration by suppressing Akt and ERK1/2 signaling pathways in human LoVo colon cancer cells</title><title>Molecular and cellular biochemistry</title><description>Epidemiological studies demonstrate that the incidence and mortality rates of colorectal cancer in women are lower than in men. However, it is unknown if 17[beta]-estradiol treatment is sufficient to inhibit prostaglandin E2 (PGE2)-induced cellular motility in human colon cancer cells. Upregulation of cyclooxygenase-2 (COX-2) is reported to associate with the development of cancer cell mobility, metastasis, and subsequent malignant tumor. After administration of inhibitors including LY294002 (Akt activation inhibitor), U0126 (ERK1/2 inhibitor), SB203580 (p38 MAPK inhibitor), SP600125 (JNK1/2 inhibitor), or QNZ (NF[kappa]B inhibitor), we found that PGE2 treatment increases COX-2 via Akt and ERK1/2 pathways, thus promoting cellular motility in human LoVo cancer cells. We further observed that 17[beta]-estradiol treatment inhibits PGE2-induced COX-2 expression and cellular motility via suppressing activation of Akt and ERK1/2 in human LoVo cancer cells. Collectively, these results suggest that 17[beta]-estradiol treatment dramatically inhibits PGE2-induced progression of human LoVo colon cancer cells. Keywords Estrogen * Prostaglandin E2 * Human colon cancer cell * COX-2 * Cell motility</description><subject>Biochemistry</subject><subject>Cancer cells</subject><subject>Cell adhesion & migration</subject><subject>Colon cancer</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>COX-2 inhibitors</subject><subject>Estradiol</subject><subject>Estrogens</subject><subject>Gene expression</subject><subject>Health aspects</subject><subject>Kinases</subject><subject>Phenols</subject><subject>Prostaglandins E</subject><subject>Signal 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Hsi-Hsien</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>17[beta]-Estradiol inhibits prostaglandin E2-induced COX-2 expressions and cell migration by suppressing Akt and ERK1/2 signaling pathways in human LoVo colon cancer cells</atitle><jtitle>Molecular and cellular biochemistry</jtitle><date>2010-09-01</date><risdate>2010</risdate><volume>342</volume><issue>1-2</issue><spage>63</spage><pages>63-</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Epidemiological studies demonstrate that the incidence and mortality rates of colorectal cancer in women are lower than in men. However, it is unknown if 17[beta]-estradiol treatment is sufficient to inhibit prostaglandin E2 (PGE2)-induced cellular motility in human colon cancer cells. Upregulation of cyclooxygenase-2 (COX-2) is reported to associate with the development of cancer cell mobility, metastasis, and subsequent malignant tumor. After administration of inhibitors including LY294002 (Akt activation inhibitor), U0126 (ERK1/2 inhibitor), SB203580 (p38 MAPK inhibitor), SP600125 (JNK1/2 inhibitor), or QNZ (NF[kappa]B inhibitor), we found that PGE2 treatment increases COX-2 via Akt and ERK1/2 pathways, thus promoting cellular motility in human LoVo cancer cells. We further observed that 17[beta]-estradiol treatment inhibits PGE2-induced COX-2 expression and cellular motility via suppressing activation of Akt and ERK1/2 in human LoVo cancer cells. Collectively, these results suggest that 17[beta]-estradiol treatment dramatically inhibits PGE2-induced progression of human LoVo colon cancer cells. Keywords Estrogen * Prostaglandin E2 * Human colon cancer cell * COX-2 * Cell motility</abstract><cop>New York</cop><pub>Springer</pub><doi>10.1007/s11010-010-0469-7</doi></addata></record> |
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| subjects | Biochemistry Cancer cells Cell adhesion & migration Colon cancer Colorectal cancer Colorectal carcinoma COX-2 inhibitors Estradiol Estrogens Gene expression Health aspects Kinases Phenols Prostaglandins E Signal transduction |
| title | 17[beta]-Estradiol inhibits prostaglandin E2-induced COX-2 expressions and cell migration by suppressing Akt and ERK1/2 signaling pathways in human LoVo colon cancer cells |
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