Table 2.

Summary of literature of filamin-A in cancer metastasis

Research system	Observations	Reference
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]