| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-128 |
Sentence |
denotes |
Mutant p53 gains new function in promoting inflammatory signals by repression of the secreted interleukin-1 receptor antagonist. |
| T2 |
129-198 |
Sentence |
denotes |
The TP53 tumor-suppressor gene is frequently mutated in human cancer. |
| T3 |
199-296 |
Sentence |
denotes |
Missense mutations can add novel functions (gain-of-function, GOF) that promote tumor malignancy. |
| T4 |
297-505 |
Sentence |
denotes |
Here we report that mutant (mut) p53 promotes tumor malignancy by suppressing the expression of a natural occurring anti-inflammatory cytokine, the secreted interleukin-1 receptor antagonist (sIL-1Ra, IL1RN). |
| T5 |
506-624 |
Sentence |
denotes |
We show that mutp53 but not wild-type (wt) p53 suppresses the sIL-1Ra production in conditioned media of cancer cells. |
| T6 |
625-893 |
Sentence |
denotes |
Moreover, mutp53, but not wtp53, binds physically the sIL-1Ra promoter and the protein-protein interaction with the transcriptional co-repressor MAFF (v-MAF musculoaponeurotic fibrosarcoma oncogene family, protein F) is required for mutp53-induced sIL-1Ra suppression. |
| T7 |
894-1077 |
Sentence |
denotes |
Remarkably, when exposed to IL-1 beta (IL-1β) inflammatory stimuli, mutp53 sustains a ready-to-be-activated in vitro and in vivo cancer cells' response through the sIL-1Ra repression. |
| T8 |
1078-1301 |
Sentence |
denotes |
Taken together, these results identify sIL-1Ra as a novel mutp53 target gene, whose suppression might be required to generate a chronic pro-inflammatory tumor microenvironment through which mutp53 promotes tumor malignancy. |
| T1 |
0-128 |
Sentence |
denotes |
Mutant p53 gains new function in promoting inflammatory signals by repression of the secreted interleukin-1 receptor antagonist. |
| T2 |
129-198 |
Sentence |
denotes |
The TP53 tumor-suppressor gene is frequently mutated in human cancer. |
| T3 |
199-296 |
Sentence |
denotes |
Missense mutations can add novel functions (gain-of-function, GOF) that promote tumor malignancy. |
| T4 |
297-505 |
Sentence |
denotes |
Here we report that mutant (mut) p53 promotes tumor malignancy by suppressing the expression of a natural occurring anti-inflammatory cytokine, the secreted interleukin-1 receptor antagonist (sIL-1Ra, IL1RN). |
| T5 |
506-624 |
Sentence |
denotes |
We show that mutp53 but not wild-type (wt) p53 suppresses the sIL-1Ra production in conditioned media of cancer cells. |
| T6 |
625-893 |
Sentence |
denotes |
Moreover, mutp53, but not wtp53, binds physically the sIL-1Ra promoter and the protein-protein interaction with the transcriptional co-repressor MAFF (v-MAF musculoaponeurotic fibrosarcoma oncogene family, protein F) is required for mutp53-induced sIL-1Ra suppression. |
| T7 |
894-1077 |
Sentence |
denotes |
Remarkably, when exposed to IL-1 beta (IL-1β) inflammatory stimuli, mutp53 sustains a ready-to-be-activated in vitro and in vivo cancer cells' response through the sIL-1Ra repression. |
| T8 |
1078-1301 |
Sentence |
denotes |
Taken together, these results identify sIL-1Ra as a novel mutp53 target gene, whose suppression might be required to generate a chronic pro-inflammatory tumor microenvironment through which mutp53 promotes tumor malignancy. |