Table 2 Summary of literature of filamin-A in cancer metastasis

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]