LYAR promotes colorectal cancer cell mobility by activating galectin-1 expression
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Yupeng Wu1,2,*, Ming Liu1,*, Zhuchen Li1, Xiao-Bin Wu3, Ying Wang1, Yadong Wang1, Min Nie1, Feifei Huang1, Junyi Ju1, Chi Ma1, Renxiang Tan1, Ke Zen1, Chen-Yu Zhang1, Keqin Fu2, Yu-Gen Chen3, Ming-Rong Wang4, Quan Zhao1
1The State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, 210046, China
2Anhui Research Institute for Family Planning, Anhui Research Center for Population and Birth Control, Hefei, 230031, China
3The Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210029, China
4The State Key Laboratory of Molecular Oncology, Cancer Hospital and Institute, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100021, China
*These authors have contributed equally to this work
Quan Zhao, e-mail: email@example.com
Ming-Rong Wang, e-mail: firstname.lastname@example.org
Keywords: LYAR, galectin-1, colorectal cancer, cell migration and invasion
Received: May 21, 2015 Accepted: September 14, 2015 Published: September 25, 2015
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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