Gli1 promotes colorectal cancer metastasis in a Foxm1-dependent manner by activating EMT and PI3K-AKT signaling
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Chuan Zhang1,*, Yong Wang1,*, YiFei Feng1,*, Yue Zhang1, Bing Ji1, Sen Wang1, Ye Sun1, Chunyan Zhu1, Dongsheng Zhang1, Yueming Sun1
1Colorectal Department of the First Affiliated Hospital of Nanjing Medical University , Nanjing, Jiangsu CHINA, 210029
*These authors contributed equally to this work
Yueming Sun, email: [email protected]
Keywords: colorectal cancer, Gli1, metastasis, epithelial-to-mesenchymal transition, PI3K-AKT signaling
Received: September 06, 2016 Accepted: November 08, 2016 Published: November 15, 2016
Colorectal cancer(CRC) is one of the most commonly diagnosed cancers in human beings and metastasis is the main death reason. Recently, Gli1 has been reported to be a key regulator of various cancer biologies and genes expressions. However, the detailed molecular mechanism of Gli1 in CRC metastasis remains largely unknown. In this study, we aimed to investigate the role of Gli1 in CRC metastasis. We used qRT-PCR, Immunohistochemistry and Western blot to test the expression levels of Gli1, Foxm1 and other target genes in the tissues and cells; Lentivirus stable transfection to change the expression levels of Gli1 and Foxm1; Wound-healing, cell invasion, migration assays and tail vein metastatic assay to test the role of Gli1 in CRC metastasis in vitro and vivo. We demonstrated that Gli1 was significantly overexpressed in colorectal cancer tissues and cells. Foxm1 level had a positive correlation with Gli1. Furthermore, we found that Gli1 promotes colorectal cancer cells metastasis in a Foxm1-dependent manner by activating EMT and PI3K-AKT signaling. Thus, we proved that Gli1 plays important role in CRC metastasis and provided a new visual field on the therapy of CRC metastasis.
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