| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Research Abstract |
EMT plays an important role in the tumor invasion and metastases. In human breast cancer, decreased BTG2 expression correlates with metastatic recurrence and decrease in overall survival, suggesting that suppression of BTG2 plays a critical role in disease progression. To analyze the role of BTG2 in breast cancer, BTG2 expression was knocked down in mammary epithelial cells. Suppression of BTG2 enhanced the motility of cells in vitro and enhanced tumor growth and metastasis in vivo. The effects of BTG2 knockdown were mediated through activation of HER2 and HER3, leading to elevated AKT phosphorylation. Suppression of HER activation using the lapatinib abrogated the effects of BTG2 knockdown, including the increased cell migration observed in vitro and the enhancement of tumorigenesis and metastasis in vivo. These results link BTG2-dependent effects on tumor progression, and raise the possibility that targeted inhibition of this pathway may be relevant in treatment breast cancers.
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