+ |
PROX1 | up-regulates
|
Epithelial-mesenchymal_transition |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254767 |
|
|
Homo sapiens |
Prostate Cancer Cell Line |
pmid |
sentence |
27476001 |
Our present study reveals that DAB2IP prevents EMT and metastasis of prostate cancer through targeting PROX1 gene transcription and destabilizing HIF1α protein, which provides a new insight into mechanism that DAB2IP regulates EMT and PCa metastasis. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PLAU | up-regulates
|
Epithelial-mesenchymal_transition |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252264 |
|
|
Homo sapiens |
|
pmid |
sentence |
19055748 |
Our data show that functional blockade of SNAI1 (SNAI1-dominant negative (DN)) leads to a partial re-expression of E-cadherin, and induces differential expression of EMT-related genes. This is confirmed by RT-PCR of PA system genes, where PAI-1 and uPA are decreased. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
HIF1A | up-regulates
|
Epithelial-mesenchymal_transition |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254768 |
|
|
Homo sapiens |
Prostate Cancer Cell Line |
pmid |
sentence |
27476001 |
Our present study reveals that DAB2IP prevents EMT and metastasis of prostate cancer through targeting PROX1 gene transcription and destabilizing HIF1α protein, which provides a new insight into mechanism that DAB2IP regulates EMT and PCa metastasis. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
KIFC1 | up-regulates
|
Epithelial-mesenchymal_transition |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266117 |
|
|
Homo sapiens |
|
pmid |
sentence |
33361741 |
Kinesin Family Member C1 (KIFC1) Regulated by Centrosome Protein E (CENPE) Promotes Proliferation, Migration, and Epithelial-Mesenchymal Transition of Ovarian Cancer |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
SNAI1 | up-regulates
|
Epithelial-mesenchymal_transition |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-265252 |
|
|
Homo sapiens |
HeLa Cell |
pmid |
sentence |
29305973 |
Our findings show that Snai1 mediates repression of PXDN and consolidate a role for this ECM-modifier during EMT. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252259 |
|
|
Homo sapiens |
|
pmid |
sentence |
19055748 |
Taken together these results suggest that SNAI1 functional blockade is leading to partial re-expression of E-cadherin (i.e. at the level of transcription), to a decrease in PAI-1 and to a more collective migration, while the parental cells expressing SNAI1 have less E-cadherin, more PAI 1, and migrate individually. We suggest that the present study establishes a relation between SNAI1 function, PAI-1 distribution and EMT status. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
+ |
PXDN | up-regulates
|
Epithelial-mesenchymal_transition |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-265253 |
|
|
Homo sapiens |
HeLa Cell |
pmid |
sentence |
29305973 |
Our findings show that Snai1 mediates repression of PXDN and consolidate a role for this ECM-modifier during EMT. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CDH1 | down-regulates
|
Epithelial-mesenchymal_transition |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252261 |
|
|
|
|
pmid |
sentence |
15601859 |
A hallmark characteristic of epithelial tumor progression as well as some processes of normal development is the loss of the epithelial phenotype and acquisition of a motile or mesenchymal phenotype. Such epithelial to mesenchymal transitions are accompanied by the loss of E-cadherin function by either transcriptional or posttranscriptional mechanisms. |
|
Publications: |
1 |
+ |
AXL | up-regulates activity
binding
|
Epithelial-mesenchymal_transition |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-277723 |
|
|
Homo sapiens |
Neutrophil |
pmid |
sentence |
35022267 |
Gas6 and its main receptor AXL are overexpressed in pancreatic cancer and their expression correlates with poor prognosis.Gas6/AXL signalling in cancer cells is associated with tumour cell proliferation, epithelial mesenchymal transition and metastases. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
HOOK1 | down-regulates
|
Epithelial-mesenchymal_transition |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260643 |
|
|
Homo sapiens |
A-549 Cell |
pmid |
sentence |
25331952 |
The epithelial-mesenchymal transition (EMT) is an essential process for embryogenesis. It also plays a critical role in the initiation of tumor metastasis.Overexpression of Hook1 inhibited EMT while knockdown of Hook1 promoted EMT. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
SPRY4 | down-regulates
|
Epithelial-mesenchymal_transition |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253036 |
|
|
Homo sapiens |
Non-small Cell Lung Cancer Cell |
pmid |
sentence |
20501643 |
Spry4 expression induces a reversal of the epithelial to mesenchymal transition characteristic of tumor cells. Treatment of a non-transformed lung epithelial cell line with shRNA to Spry4 led to decreased expression of epithelial markers and increased cell growth, supporting the concept of Spry4 acting as a tumor suppressor. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
STAT3 | up-regulates
|
Epithelial-mesenchymal_transition |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-277690 |
|
|
Homo sapiens |
|
pmid |
sentence |
26738736 |
Collectively, the activation of IL-6/STAT3 pathway contributed to the PSCs-induced EMT i |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Fibroblast |