https://scholars.lib.ntu.edu.tw/handle/123456789/391019
標題: | Sonic hedgehog pathway inhibitor mitigates mouse hepatocellular carcinoma | 作者: | CHI-JUEI JENG | 關鍵字: | GDC-0449; Gli-1; Ptch-1; Shh; Smo; Sonic hedgehog pathway | 公開日期: | 2015 | 卷: | 210 | 期: | 3 | 起(迄)頁: | 554-560 | 來源出版物: | American journal of surgery | 摘要: | Background Hepatocellular carcinoma (HCC) is a leading cause of death in Asian countries. Sonic hedgehog (Shh) pathway plays a role in hepatocarcinogenesis. We investigated the treatment effect of mouse HCC with Shh inhibitor GDC-0449. Methods Mouse hepatoma ML-1 cells were implanted in B6 mice. Fifteen days later, GDC-0449 (vismodegib), antagonist of smoothened, was used to treat HCC-bearing mice. The tumor size and liver histopathological features were analyzed, as well as gene expression in Shh pathways. Results GDC-0449 treatment effectively reduced tumor size and cell infiltration of the HCC in mice. Gene expression of Shh pathway molecules was altered, including upregulated Shh expression and downregulated smoothened expression in tumor fractions after GDC-0449 treatment. Conclusion GDC-0449 could effectively mitigate HCC growth in vivo. ? 2015 Elsevier Inc. All rights reserved. |
URI: | http://www.scopus.com/inward/record.url?eid=2-s2.0-84945994105&partnerID=MN8TOARS http://scholars.lib.ntu.edu.tw/handle/123456789/391019 |
DOI: | 10.1016/j.amjsurg.2015.03.001 | SDG/關鍵字: | messenger RNA; sonic hedgehog protein; transcription factor Gli1; vismodegib; anilide; antineoplastic agent; cell surface receptor; G protein coupled receptor; GLI1 protein, human; messenger RNA; patched receptors; pyridine derivative; Shh protein, mouse; Smo protein, mouse; sonic hedgehog protein; transcription factor; vismodegib; animal cell; animal experiment; animal model; animal tissue; Article; cancer growth; cancer size; cell infiltration; controlled study; down regulation; drug efficacy; drug megadose; gene expression; histopathology; in vivo study; liver carcinogenesis; liver cell carcinoma; male; mouse; nonhuman; priority journal; protein expression; real time polymerase chain reaction; upregulation; animal; antagonists and inhibitors; C57BL mouse; Carcinoma, Hepatocellular; genetics; Liver Neoplasms, Experimental; metabolism; pathology; randomization; Anilides; Animals; Antineoplastic Agents; Carcinoma, Hepatocellular; Down-Regulation; Gene Expression; Hedgehog Proteins; Liver Neoplasms, Experimental; Male; Mice, Inbred C57BL; Pyridines; Random Allocation; Receptors, Cell Surface; Receptors, G-Protein-Coupled; RNA, Messenger; Transcription Factors; Up-Regulation |
顯示於: | 醫學院附設醫院 (臺大醫院) |
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