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.