Institute of Traumatic Brain Injury and Nervous Diseases of Chinese People's Armed Police Forces, Center for Neurology and Neurosurgery of Affiliated Hospital of Logistics College of CPAPF, Tianjin, China.
PLoS One. 2013 Aug 26;8(8):e72376. doi: 10.1371/journal.pone.0072376. eCollection 2013.
Forkhead box M1 (FoxM1) is a member of the forkhead transcription factor family and is overexpression in malignant gliomas. However, the molecular mechanisms by which FoxM1lead to glioma carcinogenesis and progression are still not well known. In the present study, we show that Anxa1 was overexpression in gliomas and predicted the poor outcome. Furthermore, Anxa1 closely related to the FoxM1 expression and was a direct transcriptional target of FoxM1. Overexpression of FoxM1 up-regulated Anxa1 expression, whereas suppression of FoxM1 expression down-regulated Anxa1 expression in glioma cells. Finally, FoxM1 enhanced the proliferation, migration, and angiogenesis in Anxa1-dependent manner both in vitro and in vivo. Our findings provide both clinical and mechanistic evidences that FoxM1 contributes to glioma development by directly up-regulating Anxa1 expression.
叉头框转录因子 M1（FoxM1）是叉头转录因子家族的一员，在恶性胶质瘤中过度表达。然而，FoxM1 导致胶质瘤发生和进展的分子机制尚不清楚。在本研究中，我们表明 Anxa1 在胶质瘤中过度表达，并预测预后不良。此外，Anxa1 与 FoxM1 的表达密切相关，是 FoxM1 的直接转录靶标。FoxM1 的过表达上调 Anxa1 的表达，而 FoxM1 表达的抑制下调了胶质瘤细胞中 Anxa1 的表达。最后，FoxM1 在体外和体内以依赖 Anxa1 的方式增强了增殖、迁移和血管生成。我们的研究结果提供了临床和机制证据，表明 FoxM1 通过直接上调 Anxa1 的表达促进胶质瘤的发展。
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