| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-116 |
Sentence |
denotes |
Activation of VCAM-1 and its associated molecule CD44 leads to increased malignant potential of breast cancer cells. |
| T1 |
0-116 |
Sentence |
denotes |
Activation of VCAM-1 and its associated molecule CD44 leads to increased malignant potential of breast cancer cells. |
| TextSentencer_T2 |
117-324 |
Sentence |
denotes |
VCAM-1 (CD106), a transmembrane glycoprotein, was first reported to play an important role in leukocyte adhesion, leukocyte transendothelial migration and cell activation by binding to integrin VLA-1 (α4β1). |
| T2 |
117-324 |
Sentence |
denotes |
VCAM-1 (CD106), a transmembrane glycoprotein, was first reported to play an important role in leukocyte adhesion, leukocyte transendothelial migration and cell activation by binding to integrin VLA-1 (α4β1). |
| TextSentencer_T3 |
325-554 |
Sentence |
denotes |
In the present study, we observed that VCAM-1 expression can be induced in many breast cancer epithelial cells by cytokine stimulation in vitro and its up-regulation directly correlated with advanced clinical breast cancer stage. |
| T3 |
325-554 |
Sentence |
denotes |
In the present study, we observed that VCAM-1 expression can be induced in many breast cancer epithelial cells by cytokine stimulation in vitro and its up-regulation directly correlated with advanced clinical breast cancer stage. |
| TextSentencer_T4 |
555-792 |
Sentence |
denotes |
We found that VCAM-1 over-expression in the NMuMG breast epithelial cells controls the epithelial and mesenchymal transition (EMT) program to increase cell motility rates and promote chemoresistance to doxorubicin and cisplatin in vitro. |
| T4 |
555-792 |
Sentence |
denotes |
We found that VCAM-1 over-expression in the NMuMG breast epithelial cells controls the epithelial and mesenchymal transition (EMT) program to increase cell motility rates and promote chemoresistance to doxorubicin and cisplatin in vitro. |
| TextSentencer_T5 |
793-1040 |
Sentence |
denotes |
Conversely, in the established MDAMB231 metastatic breast cancer cell line, we confirmed that knockdown of endogenous VCAM-1 expression reduced cell proliferation and inhibited TGFβ1 or IL-6 mediated cell migration, and increased chemosensitivity. |
| T5 |
793-1040 |
Sentence |
denotes |
Conversely, in the established MDAMB231 metastatic breast cancer cell line, we confirmed that knockdown of endogenous VCAM-1 expression reduced cell proliferation and inhibited TGFβ1 or IL-6 mediated cell migration, and increased chemosensitivity. |
| TextSentencer_T6 |
1041-1191 |
Sentence |
denotes |
Furthermore, we demonstrated that knockdown of endogenous VCAM-1 expression in MDAMB231 cells reduced tumor formation in a SCID xenograft mouse model. |
| T6 |
1041-1191 |
Sentence |
denotes |
Furthermore, we demonstrated that knockdown of endogenous VCAM-1 expression in MDAMB231 cells reduced tumor formation in a SCID xenograft mouse model. |
| TextSentencer_T7 |
1192-1300 |
Sentence |
denotes |
Signaling studies showed that VCAM-1 physically associates with CD44 and enhances CD44 and ABCG2 expression. |
| T7 |
1192-1300 |
Sentence |
denotes |
Signaling studies showed that VCAM-1 physically associates with CD44 and enhances CD44 and ABCG2 expression. |
| TextSentencer_T8 |
1301-1495 |
Sentence |
denotes |
Our findings uncover the possible mechanism of VCAM-1 activation facilitating breast cancer progression, and suggest that targeting VCAM-1 is an attractive strategy for therapeutic intervention. |
| T8 |
1301-1495 |
Sentence |
denotes |
Our findings uncover the possible mechanism of VCAM-1 activation facilitating breast cancer progression, and suggest that targeting VCAM-1 is an attractive strategy for therapeutic intervention. |