期刊
CARCINOGENESIS
卷 34, 期 6, 页码 1370-1381出版社
OXFORD UNIV PRESS
DOI: 10.1093/carcin/bgt040
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资金
- National Science Council of Taiwan [NSC 101-2628-B-037-001-MY3]
- Excellence for Cancer Research Center Grant, the Department of Health, Executive Yuan, Taipei, Taiwan [DOH101-TD-C-111-002]
- Kaohsiung Medical University Research Foundation [KMUER0011]
Lung cancer is a major cancer, leading in both incidence and mortality in the world, and metastasis underlies the majority of lung cancerrelated deaths. Galectin-1, a glycan-binding protein, has been shown to be overexpressed in lung cancer and involved in tumor-mediated immune suppression. However, the functional role of galectin-1 in lung cancer per se remains unknown. We demonstrate that ectopic expression of galectin-1 in a low-metastatic CL1-0 lung cancer cell line promotes its migration, invasion and epithelial-mesenchymal transition. Conversely, we also show that suppression of galectin-1 expression in highly invasive CL1-5 and A549 cells inhibits migration and invasion of lung cancer cell and causes a mesenchymal-epithelial transition. These effects may be transduced by increasing the expression of integrin 64 and Notch1/Jagged2, which in turn co-operates in the phosphorylation of AKT. The effects of galectin-1 on cancer progression are reduced when integrin 4 and Notch1 are absent. Further study has indicated that galectin-1 knockdown prevents the spread of highly metastatic Lewis lung carcinoma in vivo. Our study suggests that galectin-1 represents a crucial regulator of lung cancer metastasis. Thus, the detection and targeted treatment of galectin-1-expressing cancer serves as a new therapeutic target for lung cancer.
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