title: Id-1 promotes osteosarcoma cell growth and inhibits cell apoptosis via PI3K/AKT signaling pathway.
abstract: Accumulating evidence reveals that Id-1 is upregulated and functions as a potential tumor promoter in several human cancer types. However, the role of Id-1 in osteosarcoma (OS) is unknown. In present study, we found that Id-1 expression was elevated in OS tissues than adjacent normal bone tissues. More importantly, we demonstrated that overexpression of Id-1 is significantly correlated with tumor progression and poor survival in OS patients. Furthermore, increased expression of Id-1 was observed in OS cell lines and ectopic expression of Id-1 significantly enhanced in vitro cell proliferation and promoted in vivo tumor growth, whereas knockdown of Id-1 suppressed OS cells growth. Moreover, our experimental data revealed that Id-1 promotes cell proliferation by facilitating cell cycle progression and inhibits cell apoptosis. Mechanistically, the effects of Id-1 in OS cells is at least partly through activation of PI3K/Akt signaling pathway. Therefore, we identified a tumorigenic role of Id-1 in OS and suggested a potential therapeutic target for OS patients.
authors.affiliation: Department of Orthopaedic Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang 300006, China.
authors.forename: Liang
authors.initials: L
authors.lastname: Hao
authors.affiliation: Department of Orthopaedic Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang 300006, China.
authors.forename: Qi
authors.initials: Q
authors.lastname: Liao
authors.affiliation: Department of Orthopaedic Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang 300006, China.
authors.forename: Qiang
authors.initials: Q
authors.lastname: Tang
authors.affiliation: Department of Pathology, The Fourth Affiliated Hospital of Nanchang University, Nanchang 330006, China.
authors.forename: Huan
authors.initials: H
authors.lastname: Deng
authors.affiliation: Department of Orthopaedic Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang 300006, China. Electronic address: chenlu0578@163.com.
authors.forename: Lu
authors.initials: L
authors.lastname: Chen
mesh_terms: D017209:Apoptosis; D001859:Bone Neoplasms / Q000378:metabolism* / Q000473:pathology; D063646:Carcinogenesis / Q000378:metabolism* / Q000473:pathology; D049109:Cell Proliferation; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D051798:Inhibitor of Differentiation Protein 1 / Q000378:metabolism*; D012516:Osteosarcoma / Q000378:metabolism* / Q000473:pathology; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D015398:Signal Transduction; D014407:Tumor Cells, Cultured
chemical_list: C497453:ID1 protein, human; D051798:Inhibitor of Differentiation Protein 1; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt
keywords: Apoptosis; Id-1; Osteosarcoma; PI3K/AKT pathway; Proliferation