Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 235, Issue 2, Pages 932-943Publisher
WILEY
DOI: 10.1002/jcp.29008
Keywords
apoptosis; breast cancer stem cell; KDM7A; stem cell maintenance
Categories
Funding
- Innovation Fund from Joint Research Center for Precision Medicine [IFPM2016B001]
- National Natural Science Foundation of China [81672624, 81772817]
- Shanghai University of Medicine Health Science Seed Fund [SFP-18-21-15004]
- Special Program for Collaborative Innovation in Shanghai University of Medicine & Health Sciences [SPCI-17-15-001]
- Shanghai Municipal Health and Family Planning Commission of Science and Research Fund [20164Y0274, 201540090, 20174Y0004]
- Fengxian District Science and Technology Committee fund [20170801]
Ask authors/readers for more resources
Histone demethylase KDM7A regulates neuronal differentiation and development in mammals. In this study, we found that KDM7A was also required for breast cancer stem cells (BCSCs) maintenance. Silencing KDM7A significantly reduced the BCSCs population and mamosphere formation in vitro, and inhibited breast tumor growth in vivo. Restoring KDM7A expression rescued the defect in stem cell maintenance. Our mechanism analysis suggested that KDM7A upregulated the stemness-associated factors KLF4 and c-MYC for BCSCs maintenance. In addition, KDM7A knockdown promoted apoptosis through decreasing BCL2 expression and BAD phosphorylation in breast cancer (BrCa). Furthermore, restoring KDM7A and BCL2 expression rescued apoptosis inhibition in breast cancer, suggesting that KDM7A inhibited apoptosis by upregulating the BCL2 level in breast cancer. In conclusion, KDM7A promotes cancer stem cell maintenance and apoptosis inhibition in breast cancer.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available