Ghrelin induces cell migration through GHS-R, CaMKII, AMPK and NF-kappaB signaling pathway in glioma cells

ASIA unversity > 醫學暨健康學院 > 生物科技學系 > 期刊論文 > Item 310904400/16622

Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/16622

Title:	Ghrelin induces cell migration through GHS-R, CaMKII, AMPK and NF-kappaB signaling pathway in glioma cells
Authors:	蔡政芳;Tsai, Cheng-Fang
Contributors:	生物科技學系
Keywords:	GHRELIN;MIGRATION;CaMKII;AMPK;NF-κB
Date:	2011-05
Issue Date:	2012-11-23 09:15:12 (UTC+0)
Abstract:	Ghrelin is a newly discovered gastric peptide which stimulates food intake, energy balance, and growth hormone release. Recent reports have also shown that circulating ghrelin can efficiently reach the brain. However, the molecular mechanisms and pathophysiologic roles underlying ghrelin-induced glioma migration remain unclear. Glioma is the most common primary adult brain tumor with poor prognosis because of the spreading of tumor cell to the other regions of brain easily. In present study, we found that application of recombinant human ghrelin enhances the glioma cell migration in both rat C6 and human U251 cells. Ghrelin and its receptor GHS-R (growth hormone secretagogue receptor) are expressed in a wide variety of tissues and cell types, including various cancer cells. However, little is known about the expression of ghrelin or GHS-R in brain tumors. Here, we found that ghrelin increased GHS-R receptor up-regulation, and the enhancement of ghrelin-induced glioma cell motility markedly inhibited by a GHS-R antagonist. In addition, ghrelin-mediated migration was attenuated by treatment of CaMKII inhibitor, and AMPK inhibitors and pre-transfection with AMPK siRNA. Moreover, ghrelin stimulation also increased the phosphorylation of CaMKII and AMPK. Treatment with three different types of NF-κB inhibitors or pre-transfection with KM-IKKα, or KM-IKKβ also reduced ghrelin-induced glioma cell migration. Moreover, treatment of ghrelin also induced IKKα/β activation, IκBα phosphorylation, p65 phosphorylation at Ser(536), and increased NF-κB-DNA binding activity and κB-transcriptional activity. These results indicate that ghrelin enhances migration of glioma cells is mainly regulated by the GHS-R, CaMKII, AMPK, and NF-κB pathway.
Relation:	JOURNAL OF CELLULAR BIOCHEMISTRY;112(10):2931-41.
Appears in Collections:	[生物科技學系] 期刊論文

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