1 Department of Oncology, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, PR China anna_1188@126.com shengren1211@126.com dxiang@bwh.harvard.edu.
2 Department of Urology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
3 College of Life and Health Sciences, Northeastern University, Shenyang, PR China.
4 Department of Oncology, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, PR China.
5 School of Medicine and Centre for Molecular and Medical Research, Deakin University, Waurn Ponds, Australia.
6 Department of Pathology, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, PR China.
7 Department of Vascular Biology, Boston Children's Hospital, Boston, MA, USA.
8 Department of General Surgery, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
9 Shanghai Center for Bioinformation Technology and Shanghai Engineering Research Center of Pharmaceutical Translation, Shanghai Industrial Technology Institute, Shanghai, PR China.
10 Department of Orthopedics, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, PR China.
11 College of Life and Health Sciences, Northeastern University, Shenyang, PR China anna_1188@126.com shengren1211@126.com dxiang@bwh.harvard.edu.
12 Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA anna_1188@126.com shengren1211@126.com dxiang@bwh.harvard.edu.
13 Department of Medicine, Harvard Medical School, Boston, MA, USA.
14 Shanghai Research Center of Biliary Tract Disease Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
This study demonstrates that CDKL3 regulates Akt activation and its downstream targets to promote OS progression, creating a therapeutically targetable vulnerability in treatment of OS.