Klezovitch Olga, Fernandez Tania E, Tapscott Stephen J, Vasioukhin Valeri
Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.
Genes Dev. 2004 Mar 1;18(5):559-71. doi: 10.1101/gad.1178004.
Disruption of cell polarity is seen in many cancers; however, it is generally considered a late event in tumor progression. Lethal giant larvae (Lgl) has been implicated in maintenance of cell polarity in Drosophila and cultured mammalian cells. We now show that loss of Lgl1 in mice results in formation of neuroepithelial rosette-like structures, similar to the neuroblastic rosettes in human primitive neuroectodermal tumors. The newborn Lgl1(-/-) pups develop severe hydrocephalus and die neonatally. A large proportion of Lgl1(-/-) neural progenitor cells fail to exit the cell cycle and differentiate, and, instead, continue to proliferate and die by apoptosis. Dividing Lgl1(-/-) cells are unable to asymmetrically localize the Notch inhibitor Numb, and the resulting failure of asymmetric cell divisions may be responsible for the hyperproliferation and the lack of differentiation. These results reveal a critical role for mammalian Lgl1 in regulating of proliferation, differentiation, and tissue organization and demonstrate a potential causative role of disruption of cell polarity in neoplastic transformation of neuroepithelial cells.
细胞极性破坏在许多癌症中都可见;然而,它通常被认为是肿瘤进展中的晚期事件。致死性巨幼虫(Lgl)已被证明与果蝇和培养的哺乳动物细胞中的细胞极性维持有关。我们现在表明,小鼠中Lgl1的缺失会导致神经上皮玫瑰花结样结构的形成,类似于人类原始神经外胚层肿瘤中的神经母细胞玫瑰花结。新生的Lgl1(-/-)幼崽会发展为严重脑积水并在出生时死亡。很大一部分Lgl1(-/-)神经祖细胞无法退出细胞周期并分化,而是继续增殖并通过凋亡死亡。正在分裂的Lgl1(-/-)细胞无法不对称地定位Notch抑制剂Numb,由此产生的不对称细胞分裂失败可能是过度增殖和缺乏分化的原因。这些结果揭示了哺乳动物Lgl1在调节增殖、分化和组织组织方面的关键作用,并证明了细胞极性破坏在神经上皮细胞肿瘤转化中的潜在致病作用。