Id |
Subject |
Object |
Predicate |
Lexical cue |
T1 |
0-132 |
Sentence |
denotes |
DNA damage-induced ephrin-B2 reverse signaling promotes chemoresistance and drives EMT in colorectal carcinoma harboring mutant p53. |
T1 |
0-132 |
Sentence |
denotes |
DNA damage-induced ephrin-B2 reverse signaling promotes chemoresistance and drives EMT in colorectal carcinoma harboring mutant p53. |
T2 |
133-246 |
Sentence |
denotes |
Mutation in the TP53 gene positively correlates with increased incidence of chemoresistance in different cancers. |
T2 |
133-246 |
Sentence |
denotes |
Mutation in the TP53 gene positively correlates with increased incidence of chemoresistance in different cancers. |
T3 |
247-452 |
Sentence |
denotes |
In this study, we investigated the mechanism of chemoresistance and epithelial-to-mesenchymal transition (EMT) in colorectal cancer involving the gain-of-function (GOF) mutant p53/ephrin-B2 signaling axis. |
T3 |
247-452 |
Sentence |
denotes |
In this study, we investigated the mechanism of chemoresistance and epithelial-to-mesenchymal transition (EMT) in colorectal cancer involving the gain-of-function (GOF) mutant p53/ephrin-B2 signaling axis. |
T4 |
453-620 |
Sentence |
denotes |
Bioinformatic analysis of the NCI-60 data set and subsequent hub prediction identified EFNB2 as a possible GOF mutant p53 target gene, responsible for chemoresistance. |
T4 |
453-620 |
Sentence |
denotes |
Bioinformatic analysis of the NCI-60 data set and subsequent hub prediction identified EFNB2 as a possible GOF mutant p53 target gene, responsible for chemoresistance. |
T5 |
621-735 |
Sentence |
denotes |
We show that the mutant p53-NF-Y complex transcriptionally upregulates EFNB2 expression in response to DNA damage. |
T5 |
621-735 |
Sentence |
denotes |
We show that the mutant p53-NF-Y complex transcriptionally upregulates EFNB2 expression in response to DNA damage. |
T6 |
736-900 |
Sentence |
denotes |
Moreover, the acetylated form of mutant p53 protein is recruited on the EFNB2 promoter and positively regulates its expression in conjunction with coactivator p300. |
T6 |
736-900 |
Sentence |
denotes |
Moreover, the acetylated form of mutant p53 protein is recruited on the EFNB2 promoter and positively regulates its expression in conjunction with coactivator p300. |
T7 |
901-1030 |
Sentence |
denotes |
In vitro cell line and in vivo nude mice data show that EFNB2 silencing restores chemosensitivity in mutant p53-harboring tumors. |
T7 |
901-1030 |
Sentence |
denotes |
In vitro cell line and in vivo nude mice data show that EFNB2 silencing restores chemosensitivity in mutant p53-harboring tumors. |
T8 |
1031-1207 |
Sentence |
denotes |
In addition, we observed high expression of EFNB2 in patients having neoadjuvant non-responder colorectal carcinoma compared with those having responder version of the disease. |
T8 |
1031-1207 |
Sentence |
denotes |
In addition, we observed high expression of EFNB2 in patients having neoadjuvant non-responder colorectal carcinoma compared with those having responder version of the disease. |
T9 |
1208-1414 |
Sentence |
denotes |
In the course of deciphering the drug resistance mechanism, we also show that ephrin-B2 reverse signaling induces ABCG2 expression after drug treatment that involves JNK-c-Jun signaling in mutant p53 cells. |
T9 |
1208-1414 |
Sentence |
denotes |
In the course of deciphering the drug resistance mechanism, we also show that ephrin-B2 reverse signaling induces ABCG2 expression after drug treatment that involves JNK-c-Jun signaling in mutant p53 cells. |
T10 |
1415-1567 |
Sentence |
denotes |
Moreover, 5-fluorouracil-induced ephrin-B2 reverse signaling promotes tumorigenesis through the Src-ERK pathway, and drives EMT via the Src-FAK pathway. |
T10 |
1415-1567 |
Sentence |
denotes |
Moreover, 5-fluorouracil-induced ephrin-B2 reverse signaling promotes tumorigenesis through the Src-ERK pathway, and drives EMT via the Src-FAK pathway. |
T11 |
1568-1826 |
Sentence |
denotes |
We thus conclude that targeting ephrin-B2 might enhance the therapeutic potential of DNA-damaging chemotherapeutic agents in mutant p53-bearing human tumors.Cell Death and Differentiation advance online publication, 23 October 2015; doi:10.1038/cdd.2015.133. |
T11 |
1568-1826 |
Sentence |
denotes |
We thus conclude that targeting ephrin-B2 might enhance the therapeutic potential of DNA-damaging chemotherapeutic agents in mutant p53-bearing human tumors.Cell Death and Differentiation advance online publication, 23 October 2015; doi:10.1038/cdd.2015.133. |