FoxM1 and Wnt/β-Catenin Signaling in Glioma Stem Cells

• Published in: Cancer research (Chicago, Ill.) Vol. 72; no. 22; pp. 5658 - 5662
• Main Authors: Gong, Aihua, Huang, Suyun
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Association for Cancer Research 15-11-2012
• Subjects: Animals; Antineoplastic agents; beta Catenin - metabolism; Biological and medical sciences; Brain Neoplasms - metabolism; Brain Neoplasms - pathology; Forkhead Box Protein M1; Forkhead Transcription Factors - metabolism; Glioma - metabolism; Glioma - pathology; Humans; Medical sciences; Neoplastic Stem Cells - metabolism; Neoplastic Stem Cells - pathology; Neurology; Pharmacology. Drug treatments; Signal Transduction; Tumors; Tumors of the nervous system. Phacomatoses; Wnt Proteins - metabolism; Nervous system diseases; Glioma; Wnt/β-catenin signaling pathway; Stem cell; Central nervous system disease; Tumor; Cell signaling
• ISSN: 0008-5472; 1538-7445
• DOI: 10.1158/0008-5472.CAN-12-0953

Cancer stem cells may be responsible for tumor initiation and maintenance. The molecular mechanisms that control cancer stem cells are related to alterations in various signaling pathways, including the Wnt/β-catenin signaling pathway. The canonical Wnt/β-catenin signaling pathway is one of the major signaling systems in stem and progenitor cells, and aberrant activation of the Wnt/β-catenin signaling pathway is common in human cancers. As with β-catenin, FoxM1 has been found to play important roles in a number of cancers. In this review, we discuss the evidence that FoxM1 affects the expression and function of a variety of genes that are critical to the survival, proliferation, invasion, angiogenesis, and self-renewal of cancer stem cells. We highlight the pivotal roles of the Wnt/β-catenin and FoxM1 signaling pathways in neural stem and progenitor cells and glioma stem cells. We also discuss the evidence for cross-talk between the β-catenin and FoxM1 signaling pathways in the regulation of the stemness and tumorigenicity of glioma stem cells.