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.