Id |
Subject |
Object |
Predicate |
Lexical cue |
T1 |
0-116 |
Sentence |
denotes |
JNK regulates HIPK3 expression and promotes resistance to Fas-mediated apoptosis in DU 145 prostate carcinoma cells. |
T2 |
117-342 |
Sentence |
denotes |
Elevated endogenous JNK activity and resistance to Fas receptor-mediated apoptosis have recently been implicated in progression of prostate cancer and can promote resistance to apoptosis in response to chemotherapeutic drugs. |
T3 |
343-474 |
Sentence |
denotes |
In addition, JNK has been demonstrated to promote transformation of epithelial cells by increasing both proliferation and survival. |
T4 |
475-695 |
Sentence |
denotes |
Although numerous studies have reported a role for JNK in promoting Fas receptor-mediated apoptosis, there is a paucity in the literature studying the antiapoptotic function of JNK during Fas receptor-mediated apoptosis. |
T5 |
696-877 |
Sentence |
denotes |
Consequently, we have used the recently described specific JNK inhibitor SP600125 and RNA interference to inhibit endogenous JNK activity in the prostate carcinoma cell line DU 145. |
T6 |
878-1050 |
Sentence |
denotes |
We demonstrated that endogenous JNK activity increased the expression of a kinase, HIPK3, that has previously been implicated in multidrug resistance in a number of tumors. |
T7 |
1051-1102 |
Sentence |
denotes |
HIPK3 has also been reported to phosphorylate FADD. |
T8 |
1103-1331 |
Sentence |
denotes |
The interaction between FADD and caspase-8 was inhibited, but abrogation of JNK activity or HIPK3 expression was found to restore this interaction and increased the sensitivity of DU 145 cells to Fas receptor-mediated apoptosis. |
T9 |
1332-1577 |
Sentence |
denotes |
In conclusion, we present novel evidence that JNK regulates the expression of HIPK3 in prostate cancer cells, and this contributes to increased resistance to Fas receptor-mediated apoptosis by reducing the interaction between FADD and caspase-8. |