Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P17931 (
galectin-3
)
2,860
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Ovarian cancer is the most lethal gynecologic disease because usually, it is lately sensed, easily acquires chemoresistance, and has a high recurrence rate. Recent studies suggest that ovarian cancer stem cells (CSCs) are involved in these malignancies. Here, we demonstrated that
galectin-3
maintains ovarian CSCs by activating the Notch1 intracellular domain (NICD1). The number and size of ovarian CSCs decreased in the absence of
galectin-3
, and overexpression of
galectin-3
increased them. Overexpression of
galectin-3
increased the resistance for cisplatin and paclitaxel-induced cell death. Silencing of
galectin-3
decreased the migration and invasion of ovarian cancer cells, and overexpression of
galectin-3
reversed these effects. The Notch signaling pathway was strongly activated by
galectin-3
overexpression in A2780 cells. Silencing of
galectin-3
reduced the levels of cleaved NICD1 and expression of the Notch target genes,
Hes1
and Hey1. Overexpression of
galectin-3
induced NICD1 cleavage and increased expression of
Hes1
and Hey1. Moreover, overexpression of
galectin-3
increased the nuclear translocation of NICD1. Interestingly, the carbohydrate recognition domain of
galectin-3
interacted with NICD1. Overexpression of
galectin-3
increased tumor burden in A2780 ovarian cancer xenografted mice. Increased expression of
galectin-3
was detected in advanced stages, compared to stage 1 or 2 in ovarian cancer patients, suggesting that
galectin-3
supports stemness of these cells. Based on these results, we suggest that targeting
galectin-3
may be a potent approach for improving ovarian cancer therapy.
...
PMID:Galectin-3 supports stemness in ovarian cancer stem cells by activation of the Notch1 intracellular domain. 2762 63
