In vitro analysis of the invasive phenotype of SUM 149, an inflammatory breast cancer cell line.
In vitro analysis of the invasive phenotype of SUM 149, an inflammatory breast cancer cell line.
复制标题
对炎症性乳腺癌细胞系的侵入性表型的体外分析。
DOI：
10.1186/1475-2867-5-11
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发表时间：
2005-04-27
影响因子：
5.8
通讯作者：
Dharmawardhane, Suranganie F.
中科院分区：
文献类型：
--
作者：
Hoffmeyer, Michaela R.;Wall, Kristin M.;Dharmawardhane, Suranganie F.
Inflammatory breast cancer (IBC) is the most lethal form of locally invasive breast cancer known. However, very little information is available on the cellular mechanisms responsible for manifestation of the IBC phenotype. To understand the unique phenotype of IBC, we compared the motile and adhesive interactions of an IBC cell line, SUM 149, to the non-IBC cell line SUM 102. Our results demonstrate that both IBC and non-IBC cell lines exhibit similar adhesive properties to basal lamina, but SUM 149 showed a marked increase in adhesion to collagen I. In vitro haptotaxis assays demonstrate that SUM 149 was less invasive, while wound healing assays show a less in vitro migratory phenotype for SUM 149 cells relative to SUM 102 cells. We also demonstrate a role for Rho and E-cadherin in the unique invasive phenotype of IBC. Immunoblotting reveals higher E-cadherin and RhoA expression in the IBC cell line but similar RhoC expression. Rhodamine phalloidin staining demonstrates increased formation of actin stress fibers and larger focal adhesions in SUM 149 relative to the SUM 102 cell line. The observed unique actin and cellular architecture as well as the invasive and adhesive responses to the extracellular matrix of SUM 149 IBC cells suggest that the preference of IBC cells for connective tissue, possibly a mediator important for the vasculogenic mimicry via tubulogenesis seen in IBC pathological specimens. Overexpression of E-cadherin and RhoA may contribute to passive dissemination of IBC by promoting cell-cell adhesion and actin cytoskeletal structures that maintain tissue integrity. Therefore, we believe that these findings indicate a passive metastatic mechanism by which IBC cells invade the circulatory system as tumor emboli rather than by active migratory mechanisms.
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Rho GTPases控制细胞运动过程中的极性，突出和粘附。
影响因子：
7.8
作者：
Nobes, C D;Hall, A
通讯作者：
Hall, A
影响因子：
2.5
作者：
Ethier, Stephen P.
通讯作者：
Ethier, Stephen P.
影响因子：
64.8
作者：
Clark, EA;Golub, TR;Hynes, RO
通讯作者：
Hynes, RO
DOI：
10.1083/jcb.148.2.253
发表时间：
2000-01-24
期刊：
The Journal of cell biology
影响因子：
--
作者：
O'Connor KL;Nguyen BK;Mercurio AM
通讯作者：
Mercurio AM
影响因子：
8
作者：
Moorman, JP;Luu, D;Hahn, CS
通讯作者：
Hahn, CS