Literatures reported the role of filamin-A in facilitating metastasis and cell locomotion
|
Meckel-Gruber syndrome patient
|
Filamin-A interacts with the cytoplasmic domain of meckelin, a transmembrane receptor, which is essential for neuronal migration and Wnt signalling
|
[111]
|
Hepatocellular carcinoma (HCC)
|
Comparative proteomics revealed that high level of filamin-A expression is associated with increased metastatic potentials of HCC cells.
|
[112]
|
Cancer tissues
|
By using a newly developed antibody that recognizes secreted variant of filamin-A, gradually increased levels of filamin-A was detected in normal breast tissue, localized and invasive breast cancer, which is associated with cancer progression.
|
[113]
|
Prostate cancer cell and tissue microarray
|
Filamin-A proteolysis results in nuclear localization of 90 kDa fragment, which is associated with decreased cancer metastasis, while elevated cytoplasmic levels of filamin-A was associated with enhanced metastatic potential
|
[114]
|
FlnA-knockdown rats
|
Filamin-A deficiency results in the abnormal migration, and then further causes disorganization of radial glia, which is the leading cause of PH pathogenesis.
|
[115]
|
NIH3T3 and HT1080 cells
|
Interaction of filamin-A with androgen receptor is essential for integrin β1 and FAK activation and cell migration induced by androgen stimulation
|
[79]
|
M2 and A7 melanoma cells
|
Filamin-A functions to stabilize cortical actin in vivo and is required for efficient cell locomotion
|
[16]
|
FlnA null mouse platelets
|
The interaction between FlnA and Syk regulates ITAM- and ITAM-like-containing receptor signaling which is essential for platelet spreading
|
[58]
|
M2 melanoma cells
|
R-Ras regulates migration through an interaction with filamin A in melanoma cells
|
[57]
|
EK-293 cells
|
Filamin A interacts with vimentin to regulation of cell adhesion to collagen through recycling beta1 integrins to cell membrane
|
[52,53]
|
Melanoma and breast cancer cells and breast cancer TMA
|
Filamin-A deficiency in melanoma and breast cancer cells reduces not only cell motility and invasiveness, but also spontaneous and systemic metastasis in nude mouse xenograft. Decreased filamin-A expression levels in cancer cells are associated with better survival of distant metastasis-free in breast cancer patients.
|
[116]
|
Literatures reported the role of filamin-A inhibiting metastasis
|
Human fibrosarcoma cells
|
Filamin-A deficiency increases matrix metalloproteinase (MMP) activity and induces MMP2 activation, enhancing the ability of cells to remodel the ECM and increasing their invasive potential
|
[108]
|
HT1080 and Jurkat cells
|
Filamins play a role in cell migration and spreading through the interactions between filamins and transmembrane or signaling proteins, which is mediated at least in part by repeat 19 to 21.
|
[117]
|
A7 melanoma cells
|
Migfilin acts as a molecular switch to disconnect filamin from integrin for regulating integrin activation and dynamics of extracellular matrix-actin linkage.
|
[71]
|
Hematopoietic cell
|
ASB2 may regulate hematopoietic cell differentiation by modulating cell spreading and actin remodeling through targeting of filamins for degradation
|
[48,118,119]
|
Chinese hamster ovary cells
|
Tight filamin binding restricts integrin-dependent cell migration by inhibiting transient membrane protrusion and cell polarization.
|
[105]
|
A7 and M2 cells
|
Co-expression of CEACAM1-L and filamin A lead to a reduced RalA activation, focal adhesion turnover and cell migration
|
[69]
|
Primary melanoma cell line
|
Wnt5A activates calpain-1, leading to the cleavage of filamin A, which results in a remodeling of the cytoskeleton and an increase in melanoma cell motility.
|
[120]
|
ErbB2 overexpressed breast cancer cells and Breast TMA |
Filamin-A deficiency in ErbB2-breast cancer cells reduces FAK turnover and cell motility. Down-regulation of filamin-A in stromal and base membrane is associated with breast cancer progression and invasive lymph node status |
[106] |