Department of Cancer Biology, Jefferson Medical Center, Thomas Jefferson University, Philadelphia, PA, USA.
Cell Cycle. 2011 Jun 15;10(12):1956-9. doi: 10.4161/cc.10.12.15800.
The mammalian homolog of the Drosophila dachshund gene (DACH1) has been reported as a tumor suppressor in human breast and prostate cancers. It downregulates the epidermal growth factor receptor (EGFR) and cyclin D1. The signaling pathway of the type 1 insulin-like growth factor receptor (IGF-IR) is known to be responsible for the development of resistance to treatment of human cancer with antibodies to the EGFR. We have asked whether DACH1 still exerts its tumor suppressor activity in cells dependent on the IGF-IR for growth. We find that in cells growing in IGF-1 (and unresponsive to EGF), DACH1 is devoid of tumor suppressor activity.
果蝇 Dachshund 基因（DACH1）的哺乳动物同源物已被报道为人类乳腺癌和前列腺癌中的肿瘤抑制因子。它下调表皮生长因子受体（EGFR）和细胞周期蛋白 D1。已知 1 型胰岛素样生长因子受体（IGF-IR）的信号通路负责对用针对 EGFR 的抗体治疗人类癌症产生耐药性。我们曾询问 DACH1 是否仍然在依赖 IGF-IR 生长的细胞中发挥其肿瘤抑制活性。我们发现，在 IGF-1 中生长的细胞（对 EGF 无反应）中，DACH1 缺乏肿瘤抑制活性。
