|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
RHAMM knockdown attenuates HBx-induced cell migration and invasion in vitro.
|
31792079 |
2020 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Finally, we sorted out the group of tumors with simultaneous strong CD44 and strong RHAMM expression, and found a statistically significant correlation with the depth of myometrial invasion and LVSI.
|
29734248 |
2019 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
RHAMM silencing using SiRNA was not only decreased the production of IL-6 and IL-8, but also inhibited the migration and invasion of RA-FLS.
|
30587175 |
2018 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Gene expression analyses showed that regulation of the cell motility receptor RHAMM by the RB/E2F pathway was critical for epithelial-mesenchymal transition, motility, and invasion by cancer cells.
|
27923835 |
2017 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
At IC50 for HAase activity inhibition (5-20 μg/ml [0.4-1.7 μM]), sHA-F significantly inhibited proliferation, motility and invasion of HYAL-1 expressing BCa cells (253J-Lung, HT1376, UMUC-3), P<0.001. sHA-F did not affect the growth of HYAL-1 non-expressing BCa (5637, RT4, T24, TCCSUP) and normal urothelial (Urotsa, SV-HUC1) cells. sHA-F treatment induced apoptosis by death receptor pathway. sHA-F downregulated transcript and/or protein levels of HA receptors (CD44, RHAMM), p-AKT, β-catenin, pβ-Catenin(S552), Snail and Twist but increased levels of pβ-Catenin(T41/S45), pGSK-3α/β(S21/S9) and E-cadherin. sHA-F also inhibited CD44/Phosphoinositide 3-kinase (PI-3K) complex formation and PI-3K activity.
|
27419371 |
2017 |
|
Tumor Cell Invasion
|
0.100 |
PosttranslationalModification
|
phenotype |
BEFREE |
<i>In vitro</i>, silencing of RHAMM inhibited CRC cell migration and invasion by 50% (p<0.01).
|
29050306 |
2017 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
CD44, a cell-adhesion molecule and HA receptor, can modulate intracellular signaling by forming complexes with RHAMM to promote invasion and metastasis of cancer cells.
|
24676428 |
2014 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Among candidate hyaluronan interacting proteins that could be responsible for the behavior we observed, we found that culture in the HA hydrogel triggers invasive PCa cells to differentially express and localize receptor for hyaluronan mediated motility (RHAMM)/CD168 which, in the absence of CD44, appears to contribute to PCa motility and invasion by interacting with the HA hydrogel components.
|
23166824 |
2012 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Accordingly, selective siRNA-mediated knockdown of HMMR in breast cancer cells substantially reduces the invasion and migration of cells.
|
22203674 |
2012 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
CD168 positivity was significantly correlated with the depth of invasion, nodal involvement, and vessel invasion (p < 0.01).
|
21435222 |
2011 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
We report here that HA-mediated CD168, a receptor for HA-mediated motility, and its downstream signal molecules, including ROK1, Gab-1, PI3K*p110alpha and eIF4E3, accelerate the progression of AI rather than androgen-dependent CaP and enhance AI cell invasion and metastasis in human bone marrow endothelial layers.
|
16864594 |
2007 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
These results indicate that CD44 and RHAMM differentially contribute to invasion of pancreatic adenocarcinoma; however, these functions still remain to be determined.
|
9816340 |
1996 |