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• W2318607788 abstract "3275 Breast cancer cells commonly metastasize to bone, but the mechanism underlying this osteotropism is not known. Studies from our laboratory suggest that gap junctional intercellular communication (GJIC) and connexin (Cx) expression profile contribute to breast cancer metastatic potential to bone. For instance, breast cancer cells express the gap junction protein Cx32 but not Cx43, whereas normal breast epithelial cells express Cx43, but not Cx32. Furthermore, expressing Cx43 in breast cancer cells reduces their metastatic potential, in vitro and in vivo, and reduces expression of bone related genes, including osteopontin (OPN), osteocalcin (OC) and Cbfa-1, that are upregulated in breast cancer cells. The mechanism by which Cx expression affects metastatic potential is unknown, but may involve the expression of proteins, associated with cancer cell adhesion, invasion and migration, including focal adhesion kinase (FAK), paxillin and CT10 regulator of kinase protein (Crk). To explore this possibility we examined the hypothesis that increasing expression of Cx43 in a breast cancer cell line MDA-MET (MET), reduces cell adhesion, migration, invasion and the expression of protein associated with these processes. Cx43 genes were transfected into MET cells and clones of transfectants (MET/Cx43+) screened by Q-RT-PCR. Four clones of MET/Cx43+, which expressed increased Cx43 mRNA levels, and plasmid control MET/HY were selected for further investigation. MET/Cx43+ mRNA levels increased 240% while Cx26 and OC mRNA levels were decreased 31% and 26%, respectively, relative to control. Cx45, Cx32, OPN and Cbfa-1 mRNA levels did not change significantly. Western blot analysis revealed that protein levels of FAK and paxillin in MET/Cx43+ were decreased 25% and 24%, respectively, relative to control, but there was no change in CrkI or CrkII protein. Quantitative fluorescent dye adhesion assay and Biocoat FluoroBlok Invasion System revealed that MET/Cx43+ adhesion to osteoblastic cells (hFOB 1.19) was reduced 61% and invasiveness was reduced 20%, respectively, relative to control. Cell migration did not change significantly. This study confirms and extends our previous data suggesting that the connexin expression profile and GJIC contribute to the mechanism by which breast cancer cell metastasize to bone. More importantly, these results suggest that Cx43 expression, GJIC, or both, regulate the expression of FAK and paxillin. This in turn regulates the adhesion, migration and invasion of breast cancer cells in vitro. Therefore, increasing expression of Cx43 in breast cancer cells would be expected to decrease their ability to metastasize in vivo." @default.
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• W2318607788 date "2006-04-15" @default.
• W2318607788 modified "2023-10-01" @default.
• W2318607788 title "Increasing expression of connexin 43 in breast cancer cells reduces metastatic potential to bone by down regulation of FAK and Paxillin" @default.
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