2001
DOI: 10.1006/bbrc.2001.5470
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Metastin Suppresses the Motility and Growth of CHO Cells Transfected with Its Receptor

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Cited by 95 publications
(57 citation statements)
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“…This is in stark contrast with what was seen in CHO/GPR54 cells after exogenous exposure to kisspeptins. However, there was a significant decrease in soft agar colony formation as observed in CHO/GPR54 cells (33,34). The inability of KISS1 overexpression to inhibit motility of MDA-MB-435 cells may be due to suboptimal levels of kisspeptin secretion and/or inadequate levels of GPR54 at the cell surface.…”
Section: In Vitro Implications For Gpr54/kisspeptin and Metastasismentioning
confidence: 99%
“…This is in stark contrast with what was seen in CHO/GPR54 cells after exogenous exposure to kisspeptins. However, there was a significant decrease in soft agar colony formation as observed in CHO/GPR54 cells (33,34). The inability of KISS1 overexpression to inhibit motility of MDA-MB-435 cells may be due to suboptimal levels of kisspeptin secretion and/or inadequate levels of GPR54 at the cell surface.…”
Section: In Vitro Implications For Gpr54/kisspeptin and Metastasismentioning
confidence: 99%
“…4 More recently, it has been reported that kisspeptin or metastin, a product of the KiSS-1 gene, is thought to possess potent antimetastatic property and an orphan receptor for this protein has been detected. [7][8][9][10][11][12] Although the exact mechanism of the tumor suppressor activity of KiSS-1 is yet to be revealed, the KiSS-1 gene product has recently been shown to repress type IV collagenase (MMP-9) expression and a loss of KiSS-1 expression has been associated with loss of membrane E-cadherin expression. 4,10 Moreover, very recently it was shown that activation of a Gprotein-coupled receptor (also known as AXOR12, GPR54, or hOT7T175) by KiSS-1 peptide changed cell morphology and actin filament reorganization in NIH3T3 cells.…”
mentioning
confidence: 99%
“…если ГнРГ-нейроны сами экспрессируют ER, очевидно, что регулирующее действие эстра-диола на ГнРГ-нейроны может быть трансси-наптическим потому, что эстрадиол регулиру-ет синаптическую передачу к этим клеткам [44] и нейроны, которые считаются афферентными к ГнРГ-нейронам, экспрессируют как ER-α, так и ER-β [45][46][47][48]. Особый интерес вызывают последние ис-следования, посвященные нейромодулятору кисспептину, о возможности действия эстра-диола по механизму обратной связи при регу-ляции ГнРГ-нейронов [9,49,50]. Известно, что 30 % пациентов с идиопатическим гипогона-дотропным гипогонадизмом (ИГГ) имеют му-тации в гене GPR54, приводящие к потере его функции [12].…”
Section: роль кисспептина и его рецептора в функционировании репродукunclassified