Mortalin maintains breast cancer stem cells stemness via activation of Wnt/GSK3β/β-catenin signaling pathway |
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| Authors: | Bo Wei Jia Cao Jin-Hai Tian Chuan-Yang Yu Qi Huang Jing-Jing Yu Rong Ma Jia Wang Fang Xu Li-Bin Wang |
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| Affiliation: | 1. The General Hospital of Ningxia Medical University, Yinchuan 750004, China ; 2. Ningxia Medical University, Yinchuan 750004, China ; 3. Beijing National Biochip Research Center Sub-Center in Ningxia, General Hospital of Ningxia Medical University, Yinchuan 750004, China |
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| Abstract: | 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. |
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| Keywords: | Mortalin, breast cancer stem cells, stemness, Wnt/GSK3β /β -catenin signaling pathway, EMT |
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