Id |
Subject |
Object |
Predicate |
Lexical cue |
T1 |
0-126 |
Sentence |
denotes |
The gain-of-function mutation E76K in SHP2 promotes CAC tumorigenesis and induces EMT via the Wnt/β-catenin signaling pathway. |
T1 |
0-126 |
Sentence |
denotes |
The gain-of-function mutation E76K in SHP2 promotes CAC tumorigenesis and induces EMT via the Wnt/β-catenin signaling pathway. |
T2 |
127-196 |
Sentence |
denotes |
SHP2 is encoded by the protein tyrosine phosphatase 11 (Ptpn11) gene. |
T2 |
127-196 |
Sentence |
denotes |
SHP2 is encoded by the protein tyrosine phosphatase 11 (Ptpn11) gene. |
T3 |
197-322 |
Sentence |
denotes |
Several gain-of-function (GOF) mutations in Ptpn11 have been identified in human hematopoietic malignancies and solid tumors. |
T3 |
197-322 |
Sentence |
denotes |
Several gain-of-function (GOF) mutations in Ptpn11 have been identified in human hematopoietic malignancies and solid tumors. |
T4 |
323-425 |
Sentence |
denotes |
In addition, the mutation rate for SHP2 is the highest for colorectal cancer (CRC) among solid tumors. |
T4 |
323-425 |
Sentence |
denotes |
In addition, the mutation rate for SHP2 is the highest for colorectal cancer (CRC) among solid tumors. |
T5 |
426-613 |
Sentence |
denotes |
The E76K GOF mutation is the most common and active SHP2 mutation; however, the pathogenic effects and function of this mutation in CRC tumor progression have not been well characterized. |
T5 |
426-613 |
Sentence |
denotes |
The E76K GOF mutation is the most common and active SHP2 mutation; however, the pathogenic effects and function of this mutation in CRC tumor progression have not been well characterized. |
T6 |
614-756 |
Sentence |
denotes |
The Wnt/β-catenin (CTNNB1) signaling pathway is crucial for CRC, and excessive activation of this pathway has been observed in several tumors. |
T6 |
614-756 |
Sentence |
denotes |
The Wnt/β-catenin (CTNNB1) signaling pathway is crucial for CRC, and excessive activation of this pathway has been observed in several tumors. |
T7 |
757-976 |
Sentence |
denotes |
We used Ptpn11E76K conditional knock-in mice to study this GOF mutation in colitis-associated CRC (CAC) and used the CRC cell lines HT29 and HCT116 to determine the relationship between SHP2 and Wnt/β-catenin signaling. |
T7 |
757-976 |
Sentence |
denotes |
We used Ptpn11E76K conditional knock-in mice to study this GOF mutation in colitis-associated CRC (CAC) and used the CRC cell lines HT29 and HCT116 to determine the relationship between SHP2 and Wnt/β-catenin signaling. |
T8 |
977-1080 |
Sentence |
denotes |
Ptpn11E76K conditional knock-in mice exhibited aggravated inflammation and increased CAC tumorigenesis. |
T8 |
977-1080 |
Sentence |
denotes |
Ptpn11E76K conditional knock-in mice exhibited aggravated inflammation and increased CAC tumorigenesis. |
T9 |
1081-1256 |
Sentence |
denotes |
In vitro, SHP2E76K and SHP2WT promoted malignant biological behaviors of CRC cells and induced epithelial-mesenchymal transition (EMT) via the Wnt/β-catenin signaling pathway. |
T9 |
1081-1256 |
Sentence |
denotes |
In vitro, SHP2E76K and SHP2WT promoted malignant biological behaviors of CRC cells and induced epithelial-mesenchymal transition (EMT) via the Wnt/β-catenin signaling pathway. |
T10 |
1257-1374 |
Sentence |
denotes |
Together, our results showed that SHP2E76K acts as an oncogene that promotes the tumorigenesis and metastasis of CRC. |
T10 |
1257-1374 |
Sentence |
denotes |
Together, our results showed that SHP2E76K acts as an oncogene that promotes the tumorigenesis and metastasis of CRC. |