PT  - JOURNAL ARTICLE
AU  - He, Aina
AU  - Ma, Lanjing
AU  - Huang, Yujing
AU  - Zhang, Haijiao
AU  - Duan, Wei
AU  - Li, Zexu
AU  - Fei, Teng
AU  - Yuan, Junqing
AU  - Wu, Hao
AU  - Liu, Liguo
AU  - Bai, Yueqing
AU  - Dai, Wentao
AU  - Wang, Yonggang
AU  - Li, Hongtao
AU  - Sun, Yong
AU  - Wang, Yaling
AU  - Wang, Chunyan
AU  - Yuan, Ting
AU  - Yang, Qingcheng
AU  - Tian, Songhai
AU  - Dong, Min
AU  - Sheng, Ren
AU  - Xiang, Dongxi
TI  - CDKL3 promotes osteosarcoma progression by activating Akt/PKB
AID  - 10.26508/lsa.202000648
DP  - 2020 May 01
TA  - Life Science Alliance
PG  - e202000648
VI  - 3
IP  - 5
4099  - http://www.life-science-alliance.org/content/3/5/e202000648.short
4100  - http://www.life-science-alliance.org/content/3/5/e202000648.full
SO  - Life Sci. Alliance2020 May 01; 3
AB  - Osteosarcoma (OS) is a primary malignant bone neoplasm with high frequencies of tumor metastasis and recurrence. Although the Akt/PKB signaling pathway is known to play key roles in tumorigenesis, the roles of cyclin-dependent kinase–like 3 (CDKL3) in OS progression remain largely elusive. We have demonstrated the high expression levels of CDKL3 in OS human specimens and comprehensively investigated the role of CDKL3 in promoting OS progression both in vitro and in vivo. We found that CDKL3 regulates Akt activation and its downstream effects, including cell growth and autophagy. The up-regulation of CDKL3 in OS specimens appeared to be associated with Akt activation and shorter overall patient survival (P = 0.003). Our findings identify CDKL3 as a critical regulator that stimulates OS progression by enhancing Akt activation. CDKL3 represents both a biomarker for OS prognosis, and a potential therapeutic target in precision medicine by targeting CDKL3 to treat Akt hyper-activated OS.