Interpreted the experiments. WYQ established the animal models. JM and HY provided clinical samples and carried out the patient sample analyses. ZJH, LJ, YJF and WYQ analyzed the information. All authors read and approved the final manuscript. Ethics approval and consent to participate All experimental procedures had been authorized by the Institutional Assessment Board in the Huazhong University of Science and Technology. Written informed consent was obtained for all patient samples. The biological samples have been collected from individuals with breast cancer at Wuhan No.1 Hospital (through 2014015). The control samples had been obtained from the wholesome volunteers. The study Wax Inhibitors Related Products protocol was performed ANGPTL4 Inhibitors Related Products according to the Declaration of Helsinki and was approved by the ethics committees in the Wuhan No.1 Hospital. Consent for publication Not applicable. Competing interests The authors declare that they have no competing interests.Publisher’s noteSpringer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Dysregulation of eukaryotic translation elongation aspect 1 delta (EEF1D) in cancers has been reported; nevertheless, the function and mechanisms of EEF1D in osteosarcoma stay poorly understood. The aim of this study should be to investigate the expression and function of EEF1D in osteosarcoma and to elucidate its underlying mechanisms. Solutions: The expression of EEF1D in osteosarcomas and cell lines was evaluated by qRTPCR, Western blotting and immunohistochemistry. EEF1D knockdown applying compact interfering RNA (siRNA) was employed to analyze the role of EEF1D in osteosarcoma cell proliferation and cell cycle progression. The host signaling pathways affected by EEF1D knockdown had been detected applying PathScanintracellular signaling array kit. Benefits: The expression of EEF1D was found to be upregulated in human osteosarcoma tissues and cell lines. Its expression was positively correlated with Enneking stage and the tumor recurrence. EEF1D knockdown inhibited osteosarcoma cell proliferation, colonyforming potential, and cell cycle G2M transition in vitro. In addition, EEF1D knockdown decreased the levels of phosphoAkt, phosphomTOR, and phosphoBad proteins. Conclusions: EEF1D is upregulated in osteosarcoma and plays a tumor promoting part by facilitating AktmTOR and AktBad signaling pathways. Accordingly, EEF1D is really a potential target for cancer therapy. Keyword phrases: EEF1D, Proliferation, AktmTOR signaling pathway, Aktbad signaling pathway, OsteosarcomaBackground Osteosarcoma, essentially the most widespread principal skeletal tumor in youngsters and adolescents, is characterized by the direct formation of immature bone or osteoid tissue by tumor cells [1]. Osteosarcoma regularly affects the metaphysis of long bones, especially the distal femur, proximal tibia, and proximal humerus [2]. With the introduction of neoadjuvant chemotherapy, the 5year overall survival rate of osteosarcoma has climbed from 20 to 75 [3, 4]. Even so, regardless of analysis and advances in chemotherapy regimens, the prognosis of individuals with osteosarcoma remains highly variable and is frequently dismal during the final 3 decades owing to Correspondence: [email protected]; [email protected] Equal contributors two Institution of microsurgery for limbs, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, No. 600, Yishan Road, Shanghai 200233, China 1 Division of Orthopedics, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, No. 600, Yishan Road, Shanghai 200233,.