LYAR promotes colorectal cancer cell mobility by activating galectin-1 expression

Colorectal cancer (CRC) is one of the leading causes of cancer-related death worldwide. However, the molecular mechanisms of CRC pathogenesis are not fully understood. In this study, we report the characterization of LYAR (Ly-1 antibody reactive clone) as a key regulator of the migration and invasio...

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Bibliographic Details
Published in:Oncotarget 2015-10, Vol.6 (32), p.32890-32901
Main Authors: Wu, Yupeng, Liu, Ming, Li, Zhuchen, Wu, Xiao-Bin, Wang, Ying, Wang, Yadong, Nie, Min, Huang, Feifei, Ju, Junyi, Ma, Chi, Tan, Renxiang, Zen, Ke, Zhang, Chen-Yu, Fu, Keqin, Chen, Yu-Gen, Wang, Ming-Rong, Zhao, Quan
Format: Article
Language:English
Subjects:
Binding Sites
Cell Movement
Chromatin Immunoprecipitation
Colorectal Neoplasms - genetics
Colorectal Neoplasms - metabolism
Colorectal Neoplasms - pathology
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
Galectin 1 - genetics
Galectin 1 - metabolism
Gene Expression Profiling
Gene Expression Regulation, Neoplastic
Genes, Reporter
HCT116 Cells
Humans
Immunohistochemistry
Neoplasm Invasiveness
Nuclear Proteins - genetics
Nuclear Proteins - metabolism
Promoter Regions, Genetic
Research Paper
RNA Interference
Transfection
Up-Regulation
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Summary:Colorectal cancer (CRC) is one of the leading causes of cancer-related death worldwide. However, the molecular mechanisms of CRC pathogenesis are not fully understood. In this study, we report the characterization of LYAR (Ly-1 antibody reactive clone) as a key regulator of the migration and invasion of human CRC cells. Immunohistochemistry analysis demonstrated that LYAR is expressed at a higher level in metastatic CRC tissues. We found that LYAR promoted the migratory and invasive capabilities of CRC cells. Gene expression profile analysis of CRC cells showed that LGALS1, which encodes the galectin-1 protein, was a potential target of LYAR. The ChIP assay and gene reporter assays indicated that LYAR directly bound to the LGALS1 promoter. The ectopic expression of galectin-1 partially restored the mobile potential of LYAR knocked-down cells, which suggests that galectin-1 contributed to the LYAR-promoted cell migration and invasion of CRC cells. Thus, this study revealed a novel mechanism by which the transcription factor LYAR may promote tumor cell migration and invasion by upregulating galectin-1 gene expression in CRC.
ISSN:1949-2553
1949-2553
DOI:10.18632/oncotarget.5335