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- W3149698147 abstract "Although syndecan-1 (SDC1) is known to be dysregulated in various cancer types, its implication in tumorigenesis is poorly understood. Its effect may be detrimental or protective depending on the type of cancer. Our previous data suggest that SDC1 is protective against hepatocarcinogenesis. To further verify this notion, human SDC1 transgenic (hSDC1+/+) mice were generated that expressed hSDC1 specifically in the liver under the control of the albumin promoter. Hepatocarcinogenesis was induced by a single dose of diethylnitrosamine (DEN) at an age of 15 days after birth, which resulted in tumors without cirrhosis in wild-type and hSDC1+/+ mice. At the experimental endpoint, livers were examined macroscopically and histologically, as well as by immunohistochemistry, Western blot, receptor tyrosine kinase array, phosphoprotein array, and proteomic analysis. Liver-specific overexpression of hSDC1 resulted in an approximately six month delay in tumor formation via the promotion of SDC1 shedding, downregulation of lipid metabolism, inhibition of the mTOR and the β-catenin pathways, and activation of the Foxo1 and p53 transcription factors that lead to the upregulation of the cell cycle inhibitors p21 and p27. Furthermore, both of them are implicated in the regulation of intermediary metabolism. Proteomic analysis showed enhanced lipid metabolism, activation of motor proteins, and loss of mitochondrial electron transport proteins as promoters of cancer in wild-type tumors, inhibited in the hSDC1+/+ livers. These complex mechanisms mimic the characteristics of nonalcoholic steatohepatitis (NASH) induced human liver cancer successfully delayed by syndecan-1." @default.
- W3149698147 created "2021-04-13" @default.
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- W3149698147 date "2021-03-27" @default.
- W3149698147 modified "2023-10-17" @default.
- W3149698147 title "Overexpression of Human Syndecan-1 Protects against the Diethylnitrosamine-Induced Hepatocarcinogenesis in Mice" @default.
- W3149698147 cites W12631990 @default.
- W3149698147 cites W1499046649 @default.
- W3149698147 cites W1530283338 @default.
- W3149698147 cites W1532057395 @default.
- W3149698147 cites W156547651 @default.
- W3149698147 cites W1965611273 @default.
- W3149698147 cites W1967784821 @default.
- W3149698147 cites W1970847100 @default.
- W3149698147 cites W1975689520 @default.
- W3149698147 cites W1996189137 @default.
- W3149698147 cites W1998682097 @default.
- W3149698147 cites W1999469165 @default.
- W3149698147 cites W2000440562 @default.
- W3149698147 cites W2001604240 @default.
- W3149698147 cites W2015550071 @default.
- W3149698147 cites W2021590347 @default.
- W3149698147 cites W2037038224 @default.
- W3149698147 cites W2046287218 @default.
- W3149698147 cites W2058106363 @default.
- W3149698147 cites W2063944119 @default.
- W3149698147 cites W2065575443 @default.
- W3149698147 cites W2068379194 @default.
- W3149698147 cites W2069377703 @default.
- W3149698147 cites W2072780644 @default.
- W3149698147 cites W2072948302 @default.
- W3149698147 cites W2080752012 @default.
- W3149698147 cites W2080863734 @default.
- W3149698147 cites W2088267142 @default.
- W3149698147 cites W2088442622 @default.
- W3149698147 cites W2088505684 @default.
- W3149698147 cites W2092144328 @default.
- W3149698147 cites W2095707070 @default.
- W3149698147 cites W2096413300 @default.
- W3149698147 cites W2098276373 @default.
- W3149698147 cites W2115959117 @default.
- W3149698147 cites W2117548386 @default.
- W3149698147 cites W2122770044 @default.
- W3149698147 cites W2123277882 @default.
- W3149698147 cites W2151529426 @default.
- W3149698147 cites W2154931831 @default.
- W3149698147 cites W2156563694 @default.
- W3149698147 cites W2158081651 @default.
- W3149698147 cites W2159959764 @default.
- W3149698147 cites W2161601174 @default.
- W3149698147 cites W2253541563 @default.
- W3149698147 cites W2290411490 @default.
- W3149698147 cites W2294090452 @default.
- W3149698147 cites W2316822141 @default.
- W3149698147 cites W2338361728 @default.
- W3149698147 cites W2441304977 @default.
- W3149698147 cites W2537623931 @default.
- W3149698147 cites W2553730830 @default.
- W3149698147 cites W2580015445 @default.
- W3149698147 cites W2590999575 @default.
- W3149698147 cites W2593709873 @default.
- W3149698147 cites W2767326431 @default.
- W3149698147 cites W2782529187 @default.
- W3149698147 cites W2784364369 @default.
- W3149698147 cites W2790223572 @default.
- W3149698147 cites W2901699924 @default.
- W3149698147 cites W2920475324 @default.
- W3149698147 cites W2923671338 @default.
- W3149698147 cites W2942472270 @default.
- W3149698147 cites W2956864614 @default.
- W3149698147 cites W2966901905 @default.
- W3149698147 cites W2994808807 @default.
- W3149698147 cites W3006029259 @default.
- W3149698147 cites W3021793925 @default.
- W3149698147 cites W3023457686 @default.
- W3149698147 cites W3040909370 @default.
- W3149698147 cites W3084054647 @default.
- W3149698147 cites W3087133080 @default.
- W3149698147 cites W3088954717 @default.
- W3149698147 cites W3120949185 @default.
- W3149698147 cites W4247565594 @default.
- W3149698147 doi "https://doi.org/10.3390/cancers13071548" @default.