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- W2023501811 abstract "Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FLAnnexin A6 (AnxA6) is a member of the annexin family of Ca2+-dependent membrane binding proteins that is frequently detected in cell-derived exosomes and on the surface of some cell types. Although its extracellular functions remain unclear, AnxA6 may play important roles in cell-cell and/or cell-extracellular matrix (ECM) interactions via its interactions with chondroitin sulfate containing proteoglycans, the serum glycoprotein fetuin-A and other undefined extracellular matrix components. In support of this notion, recent studies have shown that depletion of AnxA6 in MDA-MB-436 breast cancer cells promoted anchorage-independent cell growth. Here we show that depletion of AnxA6 in BT-549 breast carcinoma cells not only led to impaired cell-cell cohesion and cell spreading onto collagen type IV but also inhibited cell motility and invasiveness. In 3D cultures in growth factor-reduced matrigel, AnxA6-depleted BT-549 cells formed spheroid colonies as opposed to stellate colonies formed by the parental BT-549 cells. We also show that N-cadherin is up-regulated in the motility-impaired AnxA6-depleted cells, suggesting that loss of AnxA6 may uncouple cadherin-based cell-cell interactions as part of the mechanism that determines anchorage-independent cell growth and therefore tumor growth in vivo. Our data also show that the loss of contact inhibition and invasive properties in AnxA6-depleted cells may be partly due to the formation of fewer, elongated and dispersed vinculin-based focal contacts. To verify that these focal contacts may be functionally defective, we show that whereas the MAP kinase (ERK1/2) pathway remained constitutively active, Ca2+-dependent activation of focal adhesion kinase and the phosphoinositide-3 kinase/Akt pathway were strongly inhibited in the AnxA6-depleted BT-549 cells. These data suggest that loss of AnxA6 may promote breast cancer progression via anchorage-independent cell growth due to disruption of functional focal contacts that maintain cell-cell and/or cell-ECM interactions. Supported by grants: 1 SC1 CA134018-01 and DOD W81XWH-07-1-0254Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2119. doi:10.1158/1538-7445.AM2011-2119" @default.
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- W2023501811 date "2011-04-15" @default.
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- W2023501811 title "Abstract 2119: Role of annexin A6 in anchorage-independent growth of invasive breast cancer cells" @default.
- W2023501811 doi "https://doi.org/10.1158/1538-7445.am2011-2119" @default.
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