RT Journal Article SR Electronic T1 CDKL3 promotes osteosarcoma progression by activating Akt/PKB JF Life Science Alliance JO Life Sci. Alliance FD Life Science Alliance LLC SP e202000648 DO 10.26508/lsa.202000648 VO 3 IS 5 A1 Aina He A1 Lanjing Ma A1 Yujing Huang A1 Haijiao Zhang A1 Wei Duan A1 Zexu Li A1 Teng Fei A1 Junqing Yuan A1 Hao Wu A1 Liguo Liu A1 Yueqing Bai A1 Wentao Dai A1 Yonggang Wang A1 Hongtao Li A1 Yong Sun A1 Yaling Wang A1 Chunyan Wang A1 Ting Yuan A1 Qingcheng Yang A1 Songhai Tian A1 Min Dong A1 Ren Sheng A1 Dongxi Xiang YR 2020 UL https://www.life-science-alliance.org/content/3/5/e202000648.abstract 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.