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• W1643532382 abstract "3523 Cell invasion and metastasis are hallmarks of the cancer phenotype and account for 90% of cancer deaths; therefore, proteins that govern these processes provide attractive drug targets. We used a novel variant of the human MCF-7 breast cancer cell line, termed TMX2-28, as a model to identify new therapeutic targets for breast cancer. TMX2-28 cells have lost expression of the estrogen receptor and have a mixed basal/luminal-like gene expression signature. TMX2-28 cells are highly invasive compared to MCF-7 cells as demonstrated by their ability to invade through a reconstituted basement membrane (matrigel). TMX2-28 cells display an appearance distinct from MCF-7; yet they maintain a rounded-epithelial cell morphology suggesting an amoeboid mode of cell invasion. cDNA microarray comparison of MCF-7 and TMX2-28 cells identified 1402 differentially expressed transcripts. Screening of selected genes in both human breast carcinomas and reductive mammoplasties identified the novel expression of mitogen-inducible gene-2 (MIG2) in human breast carcinomas. MIG2 controls the localization of the protein migfilin by recruiting it from cell-cell junctions to cell-ECM adhesion sites where migfilin interacts with filamin regulating actin dynamics. MIG2 mRNA is overexpressed in TMX2-28 compared to MCF-7 (17-fold) as determined by real time RT-PCR. MIG2 mRNA levels show little expression in non-tumorigenic human mammary epithelial cell lines 184, 184A1, MCF-10A, and epithelial cells isolated from human breast milk. MIG2 gene expression was evaluated in thirty frozen human breast carcinoma specimens in which 13 of 30 showed high mRNA levels. MIG2 protein was highly expressed in 12 of 27 breast tumors and MIG2 protein showed little to no expression in most normal breast tissues from reduction mammoplasty determined by immunohistochemistry. Using siRNA to suppress the expression of MIG2 mRNA levels in TMX2-28 cells it was determined that MIG2 plays a role in cancer cell invasion and multicellular spheroid formation in 3D-matrigel cultures. TMX2-28 cell invasion was reduced by 68% when transiently transfected with siRNAs targeting MIG2 compared to cells transfected with siRNAs against GAPDH. siRNAs against MIG2 inhibited spheroid formation of TMX2-28 cells, whereas cells treated with siRNAs against GAPDH formed solid spheroids after 48 hours. Using immunofluorescence we found that MIG2 was highly localized with F-actin identified by phalloidin staining in the aggressive TMX2-28 breast cancer cells compared to nonaggressive MCF-7 cells. Furthermore, dual-immunofluorescence with the focal adhesion markers FAK and talin revealed that migfilin is highly concentrated at focal adhesion sites in TMX2-28 cells compared to MCF-7. Data from these studies suggest that targeting either MIG2 or other interacting proteins at focal adhesions may provide beneficial therapies for a subset of breast cancers." @default.
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• W1643532382 date "2006-04-15" @default.
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• W1643532382 title "MIG2 is overexpressed in human breast carcinomas and plays a role in cancer cell invasion" @default.
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