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| Home > Publications database > Kupffer Cell-Derived Tnf Triggers Cholangiocellular Tumorigenesis through JNK due to Chronic Mitochondrial Dysfunction and ROS. > print |
| Home > Publications database > Kupffer Cell-Derived Tnf Triggers Cholangiocellular Tumorigenesis through JNK due to Chronic Mitochondrial Dysfunction and ROS. > print |
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| 024 | 7 | _ | |a 10.1016/j.ccell.2017.05.006 |2 doi |
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| 100 | 1 | _ | |a Yuan, Detian |0 P:(DE-He78)b7267d2eb18316483adbd62e60d9a3ad |b 0 |e First author |
| 245 | _ | _ | |a Kupffer Cell-Derived Tnf Triggers Cholangiocellular Tumorigenesis through JNK due to Chronic Mitochondrial Dysfunction and ROS. |
| 260 | _ | _ | |a Cambridge, Mass. |c 2017 |b Cell Press |
| 336 | 7 | _ | |a article |2 DRIVER |
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| 520 | _ | _ | |a Intrahepatic cholangiocarcinoma (ICC) is a highly malignant, heterogeneous cancer with poor treatment options. We found that mitochondrial dysfunction and oxidative stress trigger a niche favoring cholangiocellular overgrowth and tumorigenesis. Liver damage, reactive oxygen species (ROS) and paracrine tumor necrosis factor (Tnf) from Kupffer cells caused JNK-mediated cholangiocellular proliferation and oncogenic transformation. Anti-oxidant treatment, Kupffer cell depletion, Tnfr1 deletion, or JNK inhibition reduced cholangiocellular pre-neoplastic lesions. Liver-specific JNK1/2 deletion led to tumor reduction and enhanced survival in Akt/Notch- or p53/Kras-induced ICC models. In human ICC, high Tnf expression near ICC lesions, cholangiocellular JNK-phosphorylation, and ROS accumulation in surrounding hepatocytes are present. Thus, Kupffer cell-derived Tnf favors cholangiocellular proliferation/differentiation and carcinogenesis. Targeting the ROS/Tnf/JNK axis may provide opportunities for ICC therapy. |
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| 700 | 1 | _ | |a Berger, Emanuel |b 2 |
| 700 | 1 | _ | |a Liu, Lei |b 3 |
| 700 | 1 | _ | |a Gross, Nina |b 4 |
| 700 | 1 | _ | |a Heinzmann, Florian |b 5 |
| 700 | 1 | _ | |a Ringelhan, Marc |b 6 |
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| 700 | 1 | _ | |a Reich, Maria |b 16 |
| 700 | 1 | _ | |a Seehawer, Marco |b 17 |
| 700 | 1 | _ | |a Leone, Valentina |b 18 |
| 700 | 1 | _ | |a Höchst, Bastian |b 19 |
| 700 | 1 | _ | |a Wohlleber, Dirk |b 20 |
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| 700 | 1 | _ | |a Prinz, Marco |b 22 |
| 700 | 1 | _ | |a Spalding, Duncan |b 23 |
| 700 | 1 | _ | |a Protzer, Ulrike |b 24 |
| 700 | 1 | _ | |a Luedde, Tom |b 25 |
| 700 | 1 | _ | |a Terracciano, Luigi |b 26 |
| 700 | 1 | _ | |a Matter, Matthias |b 27 |
| 700 | 1 | _ | |a Longerich, Thomas |b 28 |
| 700 | 1 | _ | |a Knolle, Percy |b 29 |
| 700 | 1 | _ | |a Ried, Thomas |b 30 |
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| 700 | 1 | _ | |a Heikenwälder, Mathias |0 P:(DE-He78)66ed2d4ec9bc11d29b87ac006adf85e5 |b 43 |e Last author |
| 773 | _ | _ | |a 10.1016/j.ccell.2017.05.006 |g Vol. 31, no. 6, p. 771 - 789.e6 |0 PERI:(DE-600)2074034-7 |n 6 |p 771 - 789.e6 |t Cancer cell |v 31 |y 2017 |x 1535-6108 |
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