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- 저자 : ( Jane Seon Young Kim ) (검색결과 2 건)
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( Han Byoul Cho ),( Jane Seon Young Kim ),( Hyun Soo Chung ),( Hee Jeong Lee ),( Jae Hoon Kim ) 대한산부인과학회 2012 대한산부인과학회 학술대회 Vol.98 No.-
ARID1A, the tumor suppressor gene, encodes BAF250a which is a component of human SWI/SNF chromatin-remodeling complexes and has recently reported loss of expressions in several tumor types. Here, we investigate the expression levels of the BAF250a during the sequential steps of cervical carcinogenesis and assess its prognostic value. One hundred forty seven cervical cancer patients, 191 cervical intraepithelial neoplasia, and 376 matched nonadjacent normal tissues were arrayed into tissue microarray. BAF250a expressions were assessed by immunohistochemistry (IHC) and studied the relationship between BAF250a expression and clinicopathologic parameters including survival data. The transcriptional level of BAF250a was also evaluated by SYBR Green real-time PCR in 5 cell lines and 10 clinical specimens. We showed that the mRNA expression levels of BAF250a decreased in cervical cancer cell lines (p=0.005) and tissues (p=0.001), compared with normal cervical epithelial tissues, respectively. BAF250a was detected in nuclear factions of HeLa cells and nucleus of cervical cancer tissue sample by western blotting and IHC, respectively. The expression level of BAF250a gradually decreased during the normal to tumor transition of cervical carcinoma (p<0.001), and this loss of the expression was significantly associated with tumor stage (p=0.005), tumor grade (p=0.029), tumor size (p=0.003), and lymph node metastasis (p=0.020). In multivariate analysis, overall survival in cervical cancer was significantly shorter in cases with the loss of BAF250a expression (HR = 2.78 [1.01-7.63], p=0.047). Our results suggest that BAF250a expression has the potential to provide valuable prognostic information to clinicians for risk assessment in cervical cancer.
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Mo, Jung-Soon,Ann, Eun-Jung,Yoon, Ji-Hye,Jung, Jane,Choi, Yun-Hee,Kim, Hwa-Young,Ahn, Ji-Seon,Kim, Su-Man,Kim, Mi-Yeon,Hong, Ji-Ae,Seo, Mi-Sun,Lang, Florian,Choi, Eui-Ju,Park, Hee-Sae Cambridge University Press 2011 Journal of cell science Vol.124 No.1
<P>Notch is a transmembrane protein that acts as a transcriptional factor in the Notch signaling pathway for cell survival, cell death and cell differentiation. Notch1 and Fbw7 mutations both lead the activation of the Notch1 pathway and are found in the majority of patients with the leukemia T-ALL. However, little is known about the mechanisms and regulators that are responsible for attenuating the Notch signaling pathway through Fbw7. Here, we report that the serum- and glucocorticoid-inducible protein kinase SGK1 remarkably reduced the protein stability of the active form of Notch1 through Fbw7. The protein level and transcriptional activity of the Notch1 intracellular domain (Notch1-IC) were higher in SGK1-deficient cells than in SGK1 wild-type cells. Notch1-IC was able to form a trimeric complex with Fbw7 and SGK1, thereby SGK1 enhanced the protein degradation of Notch1-IC via a Fbw7-dependent proteasomal pathway. Furthermore, activated SGK1 phosphorylated Fbw7 at serine 227, an effect inducing Notch1-IC protein degradation and ubiquitylation. Moreover, accumulated dexamethasone-induced SGK1 facilitated the degradation of Notch1-IC through phosphorylation of Fbw7. Together our results suggest that SGK1 inhibits the Notch1 signaling pathway via phosphorylation of Fbw7.</P>
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