| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-111 |
Sentence |
denotes |
MicroRNA-mediated downregulation of mTOR/FGFR3 controls tumor growth induced by Src-related oncogenic pathways. |
| T1 |
0-111 |
Sentence |
denotes |
MicroRNA-mediated downregulation of mTOR/FGFR3 controls tumor growth induced by Src-related oncogenic pathways. |
| TextSentencer_T2 |
112-262 |
Sentence |
denotes |
The tyrosine kinase c-Src is upregulated in various human cancers, but the molecular mechanisms underlying c-Src-mediated tumor growth remain unclear. |
| T2 |
112-262 |
Sentence |
denotes |
The tyrosine kinase c-Src is upregulated in various human cancers, but the molecular mechanisms underlying c-Src-mediated tumor growth remain unclear. |
| TextSentencer_T3 |
263-344 |
Sentence |
denotes |
Here we examined the involvement of microRNAs in the c-Src-mediated tumor growth. |
| T3 |
263-344 |
Sentence |
denotes |
Here we examined the involvement of microRNAs in the c-Src-mediated tumor growth. |
| TextSentencer_T4 |
345-567 |
Sentence |
denotes |
Microarray profiling revealed that c-Src activation downregulates a limited set of microRNAs, including miR-99a, which targets oncogenic mammalian target of rapamycin (mTOR) and fibroblast growth factor receptor 3 (FGFR3). |
| T4 |
345-567 |
Sentence |
denotes |
Microarray profiling revealed that c-Src activation downregulates a limited set of microRNAs, including miR-99a, which targets oncogenic mammalian target of rapamycin (mTOR) and fibroblast growth factor receptor 3 (FGFR3). |
| TextSentencer_T5 |
568-704 |
Sentence |
denotes |
Re-expression of miR-99a suppressed tumor growth of c-Src-transformed cells, and this effect was restored by the overexpression of mTOR. |
| T5 |
568-704 |
Sentence |
denotes |
Re-expression of miR-99a suppressed tumor growth of c-Src-transformed cells, and this effect was restored by the overexpression of mTOR. |
| TextSentencer_T6 |
705-896 |
Sentence |
denotes |
The downregulation of miR-99a was also observed in epidermal growth factor- and Ras-transformed cells, and it was suppressed by inhibiting the mitogen-activated protein kinase (MAPK) pathway. |
| T6 |
705-896 |
Sentence |
denotes |
The downregulation of miR-99a was also observed in epidermal growth factor- and Ras-transformed cells, and it was suppressed by inhibiting the mitogen-activated protein kinase (MAPK) pathway. |
| TextSentencer_T7 |
897-1019 |
Sentence |
denotes |
Furthermore, miR-99a downregulation is associated with mTOR/FGFR3 upregulation in various human lung cancer cells/tissues. |
| T7 |
897-1019 |
Sentence |
denotes |
Furthermore, miR-99a downregulation is associated with mTOR/FGFR3 upregulation in various human lung cancer cells/tissues. |
| TextSentencer_T8 |
1020-1100 |
Sentence |
denotes |
The tumorigenicity of these cells was suppressed by the introduction of miR-99a. |
| T8 |
1020-1100 |
Sentence |
denotes |
The tumorigenicity of these cells was suppressed by the introduction of miR-99a. |
| TextSentencer_T9 |
1101-1296 |
Sentence |
denotes |
These findings suggest that the miR-99a-mTOR/FGFR3 pathway is crucial for controlling tumor growth in a wide range of human cancers that harbor upregulation of the Src-related oncogenic pathways. |
| T9 |
1101-1296 |
Sentence |
denotes |
These findings suggest that the miR-99a-mTOR/FGFR3 pathway is crucial for controlling tumor growth in a wide range of human cancers that harbor upregulation of the Src-related oncogenic pathways. |