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TRIM59 promotes osteosarcoma progression via activation of STAT3.
Xu, Guoxing; Ma, Zhenjiang; Yang, Fei; Bai, Yanqiang; Li, Jian; Luo, Wanglin; Zhong, Jiangbo.
Affiliation
  • Xu G; Department of Orthopaedics, Jiading District Anting Hospital of Shanghai, Shanghai, 201805, China.
  • Ma Z; Shanghai Key Laboratory of Orthopaedic Implant, Department of Orthopaedics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
  • Yang F; Department of Pathology, Central Hospital Affiliated to Shandong First Medical University, Jinan, 250013, Shandong, China.
  • Bai Y; Department of Orthopaedics, Central Hospital Affiliated to Shandong First Medical University, No. 105, Jiefang Road, Jinan, 250013, Shandong, China.
  • Li J; Department of Orthopaedics, Central Hospital Affiliated to Shandong First Medical University, No. 105, Jiefang Road, Jinan, 250013, Shandong, China.
  • Luo W; Department of Orthopaedics, Jiading District Anting Hospital of Shanghai, Shanghai, 201805, China.
  • Zhong J; Department of Orthopaedics, Central Hospital Affiliated to Shandong First Medical University, No. 105, Jiefang Road, Jinan, 250013, Shandong, China. Jiangbozhong@163.com.
Hum Cell ; 35(1): 250-259, 2022 Jan.
Article in En | MEDLINE | ID: mdl-34625908
Osteosarcoma (OS) is a common, highly malignant bone tumor. Tripartite motif-containing protein 59 (TRIM59) has been identified as a potential oncogenic protein involved in the initiation and progression of various human carcinomas. Nonetheless, the possible roles and molecular mechanisms of action of TRIM59 in OS remain unclear. In this study, we found that TRIM59 expression levels were frequently upregulated in OS tissues and cell lines. TRIM59 knockdown significantly suppressed the proliferation, migration, and invasion of OS cells and promoted OS cell apoptosis, whereas TRIM59 overexpression had the opposite effects. In vivo experiments demonstrated that TRIM59 knockdown suppressed OS tumor growth and metastasis in vivo. Furthermore, we found that TRIM59 directly interacted with phospho-STAT3 in OS cells. The downregulation of STAT3 levels attenuated TRIM59-induced cell proliferation and invasion. Taken together, our results indicate that TRIM59 promoted OS progression via STAT3 activation. Therefore, our study may provide a novel therapeutic target for OS.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Bone Neoplasms / Osteosarcoma / Gene Expression / Gene Expression Regulation, Neoplastic / Intracellular Signaling Peptides and Proteins / STAT3 Transcription Factor / Tripartite Motif Proteins Type of study: Prognostic_studies Limits: Humans Language: En Journal: Hum Cell Year: 2022 Document type: Article Affiliation country: China Country of publication: Japan

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Bone Neoplasms / Osteosarcoma / Gene Expression / Gene Expression Regulation, Neoplastic / Intracellular Signaling Peptides and Proteins / STAT3 Transcription Factor / Tripartite Motif Proteins Type of study: Prognostic_studies Limits: Humans Language: En Journal: Hum Cell Year: 2022 Document type: Article Affiliation country: China Country of publication: Japan