Previous research indicated that
mortalin overexpressed in
breast cancer and contributed to
carcinogenesis.
Mortalin was also demonstrated to promote Epithelial-mesenchymal transition (EMT) and was considered as
a factor for maintaining the stemness of the cancer stem cells. However, the underlying mechanisms about
mortalin maintaining the stemness of
breast cancer stem cells (BCSCs) remain unclear. Here, we identified that increased expression of
mortalin in
breast cancer was associated with poorer overall survival rate.
Mortalin was elevated in
breast cancer cell lines and BCSC-enriched populations. Additionally, knockdown of
mortalin significantly inhibited the cell proliferation, migration and EMT, as well as sphere forming capacity and stemness genes expression. Further study revealed that
mortalin promoted EMT and maintained BCSCs stemness via activating the Wnt/GSK3β/β-
catenin signaling pathway in vivo and in vitro. Taken together, these findings unveiled the mechanism of
mortalin in maintaining and regulating the stemness of BCSCs, and may offer novel therapeutic strategies for
breast cancer treatment.