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2015 ; 6
(7
): 4936-52
Nephropedia Template TP
gab.com Text
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English Wikipedia
Galectin-3 augments tumor initiating property and tumorigenicity of lung cancer
through interaction with ?-catenin
#MMPMID25669973
Chung LY
; Tang SJ
; Wu YC
; Sun GH
; Liu HY
; Sun KH
Oncotarget
2015[Mar]; 6
(7
): 4936-52
PMID25669973
show ga
Cancer stem cells (CSCs) are comprised of a rare sub-population of cells in
tumors that have been proposed to be responsible for high recurrence rates and
resistance to chemotherapy. Galectins are highly expressed in cancers that
correlate with the aggressiveness of tumors. Galectins may also promote the
resistance of cancer cells to chemotherapy. However, the role of galectins in
CSCs remains unknown. In this study, sphere formation was used to enrich H1299
human lung CSCs that had self-renewal ability, advanced tumorigenic potential,
and that highly expressed stem/progenitor cell markers such as Oct4, Sox2, Nanog,
and CD133. A novel candidate molecule, galectin-3, for stemness was found in lung
CSCs. The expression of galectin-3 robustly increased in lung cancer spheres over
serial passages, but its suppression in the H1299 monolayer or spheres resulted
in reduced expression of stemness-related genes, sphere-forming ability,
tumorigenicity, chemoresistance, and tumor initiation in mice. Notably, the
overexpression of galectin-3 in A549 lung cancer cells, which have low capability
to grow as tumor spheres, promoted CSC formation. ?-catenin activity was
increased in H1299 spheres and counteracted by galectin-3 suppression. Thus,
galectin-3 may act as a cofactor by interacting with ?-catenin to augment the
transcriptional activities of stemness-related genes. Furthermore, galectin-3
expression correlated with tumor progression and expressions of ?-catenin and CSC
marker CD133 in lung cancer tissues. Targeting galectin-3 signaling may provide a
new strategy for lung cancer treatment by inhibiting stem-like properties.