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| 1 | Enhanced migration of tissue inhibitor of metalloproteinase overexpressing hepatoma cells is attributed to gelatinases: Relevance to intracellular signaling pathways显示文摘AIM: To study the effect of gelatinases (especially MMP-9)on migration of tissue inhibitor of metalloproteinase (TIMP-1) overexpressing hepatoma cells.METHODS: Wild type HepG2 cells, cells stably transfected with TIMP-1 and TIMP-1 antagonist (MMP-9-H401A, a catalytically inactive matrix metalloproteinase (MMP) which still binds and neutralizes TIMP-1) were incubated in Boyden chambers either with or without Galardin (a synthetic inhibitor of MMP-1, -2, -3, -8, -9) or a specific inhibitor of gelatinases.RESULTS: Compared to wild type HepG2 cells, the cells overexpressing TIMP-1 showed 115% migration (P<0.05)and the cells overexpressing MMP-9-H401A showed 62% migration (P<0.01). Galardin reduced cell migration dose dependently in all cases. The gelatinase inhibitor reduced migration in TIMP-1 overexpressing cells predominantly.Furthermore, we examined intracellular signal transduction pathways of TIMP-1-dependent HepG2 cells. TIMP-1deactivates cell signaling pathways of MMP-2 and MMP-9involving p38 mitogen-activated protein kinase. Specific blockade of the ERK pathway suppresses gelatinase expression either in the presence or absence of TIMP-1.CONCLUSION: Overexpressing functional TIMP-1-enhanced migration of HepG2-TIMP-1 cells depends on enhanced MMP-activity, especially MMP-9. | Elke Roeb Anja-Katrin Bosserhoff Sabine Hamacher Bettina Jansen Judith Dahmen Sandra Wagner Siegfried Matern | 2005 | World Journal of Gastroenterology2005，11，8： | 7 |
| 2 | Reduced expression ofβ-catenin inhibitor Chibby in colon carcinoma cell lines显示文摘AIM: To analyse the Chibby expression and its function in colon carcinoma cell lines and colorectal carcinoma (CRC). METHODS: Chibby expression levels were investigated by quantitative RT-PCR in a panel of seven different colon carcinoma cell lines. By sequencing, we analysed mutational status of Chibby. To test whether Chibby exhibited effects onβ-catenin signalling in colon carcinoma cells, we transfected SW480 cells with Chibby expression plasmid and, subsequently, analysed activity of p-catenin and tested for alterations in cellular phenotype. In addition, we examined Chibby mRNA levels in samples of colorectal carcinomas and adjacent normal tissues by using quantitative RT-PCR and hybridised gene chips with samples from CRC and normal tissues. RESULTS: Chibby mRNA expression was strongly down-regulated in colon carcinoma cell lines in comparison to normal colon epithelial cells and no mutation in any of the examined colon carcinoma cell lines was found. Further, we could show that Chibby inhibited p-catenin activity in TOPflash assays when over-expressed in SW480 cells. Proliferation and invasion assays with Chibby transfected SW480 cells did not reveal profound differences compared to control cells. In contrast to these in vitro data, quantitative RT-PCR analyses of Chibby mRNA levels in CRC tumor samples did not show significant differences to specimens in adjacent non-cancerous tissue. Consistent with these findings, gene chips analysing tissue samples of tumors and corresponding normal tissue did not show altered Chibby expression CONCLUSION: Altered Chibby expression might be observed in vitro in different colon carcinoma cell lines. However, this finding could not be confirmed in vitro in CRC tumors, indicating that Chibby is not likely to promote CRC tumor development or progression. As Chibby is an important inhibitor ofβ-catenin signalling, our data implicate that the usability of colon carcinoma cell lines for in vitro studies analysing the Wnt/β-catenin pathway in colorectal carcinoma needs extensive verification. | Marion M Schuierer Elisabeth Graf Ken-Ichi Takemaru Wolfgang Dietmaier Anja-Katrin Bosserhoff | 2006 | World Journal of Gastroenterology2006，12，10： | 5 |
| 3 | Migration-associated secretion of melanoma inhibitory activity at the cell rear is supported by KCa3.1 potassium channels显示文摘恶意的黑瘤,由侵略本地生长和转移的早形成描绘了,是皮癌症的最好攻击的类型。黑瘤禁止的活动(MIA ) ,由恶意的黑瘤房间藏匿了,与房间粘附受体, integrins 伪 4 尾 1 和伪 5 尾 1,便于的房间分开和转移的支持的形成交往。在现在的学习,我们证明那 MIA 分泌物被限制到移植房间的后面的目的,当在非移居的房间 MIA 在肌动朊外皮积累时。MIA 蛋白质包括上衣蛋白质建筑群拿一条常规能分泌的小径我(COPI )- 并且上衣蛋白质建筑群 II (COPII ) 依赖者蛋白质运输到房间圆周,在它的最后的版本取决于细胞内部的 Ca2+ 离子的地方。有趣地,激活 Ca2+ 的 K+ 隧道,亚科 N,成员 4 (KCa3.1 ) ,知道在移植房间的后面的结束活跃,被发现支持 MIA 分泌物。分泌物被特定的 KCa3.1 隧道禁止者 TRAM-34 并且由隧道的主导否定的异种的表示减少。在摘要,我们阐明了到房间尾部并且也的 MIA 蛋白质的联系迁居的运输揭示了 KCa3.1 钾隧道由支持房间移植的新机制。 | Jennifer Schmidt Kristin Friebel Roland Schoenherr Marc G Coppolino Anja-Katrin Bosserhoff | 2010 | Cell Research2010，20，11： | 3 |
| 4 | Identification of novel sense and antisense transcription at the TRPM2 locus in cancer显示文摘在癌症,在染色体的体积成为 hypomethylated 的地方,可能导致能影响关键 oncosuppressor 基因的功能的 antisense 抄本的产生的 transcriptional 噪音有增加,这被建议了,最终导致恶意的转变。这里,我们描述一个充实黑瘤的 antisense 抄本的计算鉴定, TRPM2 -- 同样,在 TRPM2 的地点以内印射,能够调停的一条离子隧道危险性到房间死亡。TRPM2 的分析 -- 当 genomic 区域在另一个充实肿瘤的 TRPM2 抄本的一样的区域显示了存在, TRPM2-TE,定位了与 TRPM2 分享的一个 CpG 岛到对面 -- 作为。量的 PCR 实验证实了那 TRPM2 -- 作为并且 TRPM2-TE 抄本在黑瘤是起来调整的,并且他们的激活与分享的 CpG 岛的 methylation 地位一致。TRPM2-TE 的功能的大美人,以及野类型的 TRPM2 的在表示上,增加的黑瘤危险性到 apoptosis 和坏死。最后,在另外的癌症类型的表示分析显示了那 TRPM2 -- 作为并且 TRPM2-TE 在表示上可能比期望有一个甚至更宽的角色,在识别新潜力增强我们的计算途径的关联治疗学的目标。 | Ugo Orfanelli Ann-Kathrin Wenke Claudio Doglloni Vincenzo Russo Anja Katrin Bosserhoff Giovanni Lavorgna | 2008 | Cell Research2008，18，11： | 2 |
| 5 | p38MAPK mediates IL-1-induced down-regulation of aggrecan gene expression in human chondrocytes显示文摘 | Radons J Bosserhoff AK Grassel S | | 0，，04： | 1 |
| 6 | Integrin βexpression is regulated by let-7a miRNA in malignant melanoma显示文摘 | Muller DW Bosserhoff AK | 2008 | Oncogene2008，27，2： | 1 |
| 7 | Keratinocyte - derived cytokines after photodynamic therapy and their paracrine induction of matrix metallopmteinases in fibroblasts 显示文摘 | Karrer S Bosserhoff AK Weiderer P | 2004 | Br J Dermatol2004，151，4： | 1 |
| 8 | The-2518 promotor polymorphism in the MCP-1 gene is associated with systemic sclerosis显示文摘 | Karrer S Bosserhoff AK Weiderer P | | 0，，01： | 1 |
| 9 | Obesity and fatty liverare ‘ grease’ for the machinery of hepatic fibrosis显示文摘 | Bosserhoff A Hellerbrand C | 2011 | Dig Dis2011，29，： | 1 |
| 10 | Cloning and characterization of the expression pattern of a novel splice product MIA/CD-RAP of malignant melanoma-derived growth-inhibiting activity (MIA/CD-RAP) 显示文摘 | Hau P Wise P Bosserhoff A | 2002 | J Invest Dermatol2002，119，3： | 1 |
| 11 | Characterization and expression pattern of the novel MIA homolog TANGO显示文摘 | Bosserhoff AK Moser M Buettner R | 2004 | Gene Expr Patterns2004，4，4： | 1 |
| 12 | Integrin beta 3 expression is regulated by let-7a miRNA in malignant melanoma显示文摘 | Muller DW Bosserhoff AK | 2008 | Oncogene2008，27，52： | 1 |
| 13 | Role of miRNAs in the progression of malignant melanoma显示文摘 | Mueller DW Bosserhoff AK | 2009 | Br J Cancer2009，101，4： | 1 |
| 14 | 显示文摘 | Doris Klee Zahida Ademovic Anja Bosserhoff | 2003 | Biomaterials2003，24，： | 1 |
| 15 | Ke- ratinocyte-derived cytokines after photodynamic thcrdp?,- and their paracrine induction of matrix metalloprotcinases in fibroblasts显示文摘 | KARRER S BOSSERHOFF AK WEIDERER P | 2004 | British Journal of Dermatology2004，151，4： | 1 |
| 16 | Characterization and expression pattern of the novel MIA homolog TANGO显示文摘 | Bosserhoff AK Moser M Buettner R | 2004 | Gene expression patterns2004，4，4： | 1 |
| 17 | Mapping ATP-binding cassette transporter gene expression profiles in melanoeytes and melanoma cells显示文摘 | Heimerl S Bosserhoff AK Langmann T | 2007 | Melanoma Res2007，17，5： | 1 |
| 18 | MIA as a reliable tumor marker in the serum of patients with malignant melanoma显示文摘 | Stahlecker J Gauger A Bosserhoff A | 2000 | Anticancer Res2000，20，6： | 1 |
| 19 | A new technique for testing theimpact load of thin films:the coating impact test显示文摘 | Knotek O Bosserhoff B Schrey A | 1992 | Surface and Coatings technology1992，5455，： | 1 |
| 20 | The evolving concept of 'melano-miRs'- microRNAs in melanoma genesis 显示文摘 | Mueller DW Bosserhoff AK | 2010 | Pigment Cell Melanoma Rcs2010，23，： | 1 |
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