LYAR promotes colorectal cancer cell mobility by activating galectin-1 expression
Author(s) -
Yupeng Wu,
Ming Liu,
Zhuchen Li,
Xiaobin Wu,
Ying Wang,
Yadong Wang,
Min Nie,
Feifei Huang,
Junyi Ju,
Chi Ma,
Renxiang Tan,
Ke Zen,
ChenYu Zhang,
FU Ke-qin,
Yugen Chen,
MingRong Wang,
Quan Zhao
Publication year - 2015
Publication title -
oncotarget
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.373
H-Index - 127
ISSN - 1949-2553
DOI - 10.18632/oncotarget.5335
Subject(s) - colorectal cancer , medicine , cancer research , galectin 3 , cancer , oncology
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.
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