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 He, Aina
A1 Ma, Lanjing
A1 Huang, Yujing
A1 Zhang, Haijiao
A1 Duan, Wei
A1 Li, Zexu
A1 Fei, Teng
A1 Yuan, Junqing
A1 Wu, Hao
A1 Liu, Liguo
A1 Bai, Yueqing
A1 Dai, Wentao
A1 Wang, Yonggang
A1 Li, Hongtao
A1 Sun, Yong
A1 Wang, Yaling
A1 Wang, Chunyan
A1 Yuan, Ting
A1 Yang, Qingcheng
A1 Tian, Songhai
A1 Dong, Min
A1 Sheng, Ren
A1 Xiang, Dongxi
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.