Journal
ONCOTARGET
Volume 6, Issue 5, Pages 3111-3122Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.3076
Keywords
galectin-1; CD133; lung adenocarcinoma; Cancer Stem Cells
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Funding
- National Natural Science Foundation of China [81101775]
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Previous studies demonstrated that a subpopulation of cancer cells, which are CD133 positive (CD133(+)) feature higher invasive and metastatic abilities, are called cancer stem cells (CSCs). By using tumor cells derived from patients with lung adenocarcinoma, we found that galectin-1 is highly overexpressed in the CD133(+) cancer cells as compared to the normal cancer cells (CD133(-)) from the same patients. We overexpressed galectin-1 in CD133(-) cancer cells and downregulated it in CSCs. We found that overexpression of galectin-1 promoted invasiveness of CD133(-) cells, while knockdown of galectin-1 suppressed proliferation, colony formation and invasiveness of CSCs. Furthermore, tumor growth was significantly inhibited in CSCs xenografts with knockdown of galectin-1 as compared to CSCs treated with scramble siRNAs. Biochemical studies revealed that galectin-1 knockdown led to the suppression of COX-2/ PGE2 and AKT/ mTOR pathways, indicating galectin-1 might control the phenotypes of CSCs by regulating these signaling pathways. Finally, a retrospective study revealed that galectin-1 levels in blood circulation negatively correlates with overall survival and positively correlates with lymph node metastasis of the patients. Taken together, these findings suggested that galectin-1 plays a major role on the tumorigenesis and invasiveness of CD133(+) cancer cells and might serve as a potential therapeutic target for treatment of human patients with lung adenocarcinoma.
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