Upregulation of ALDH1B1 promotes tumor progression in osteosarcoma
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Xin Wang1,*, Yan Yu2,*, Yuting He2,*, Qiqing Cai1, Songtao Gao1, Weitao Yao1, Zhiyong Liu1, Zhichao Tian1, Qicai Han3, Weiwei Wang4, Ranran Sun2, Yonggang Luo3 and Chao Li1
1Department of Bone and Soft Tissue, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou 450008, China
2Precision Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China
3Key Laboratory of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China
4Department of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China
*These authors have contributed equally to this work
Chao Li, email: [email protected]
Yonggang Luo, email: [email protected]
Keywords: osteosarcoma; ALDH1B1; progression; proliferation; metastasis
Received: August 21, 2017 Accepted: December 04, 2017 Published: December 20, 2017
Osteosarcoma (OS) is the most common primary malignant bone tumor in childhood and adolescence with poor prognosis. The mechanism underlying tumorigenesis and development of OS is largely unknown. ALDH1B1 has been reported to involve in many kinds of human cancers and functions as an oncogene, but the role of ALDH1B1 in OS has not been investigated comprehensively. In the present study, we aimed to examine clinical value and biological function of ALDH1B1 in OS. Firstly, we investigated the roles of ALDH1B1 on an OS tissue microarray (TMA) as well as two OS cohorts from GEO database. We found that ALDH1B1 was significantly up-regulated in OS tissues and was independently associated with poor prognosis. Moreover, ALDH1B1 silencing could suppress the proliferation, migration, invasion in vitro and inhibit the growth of xenograft tumor and of OS cells in vivo. Additional, ALDH1B1 knockdown increased the apoptosis rate and lead to cell cycle arrest in G1 stage of OS cell in vitro. More importantly, the inhibition of ALDH1B1 expression could increase the sensitivity of OS cells to chemotherapy, which suggested that ALDH1B1 might be served as a therapeutic target to reverse drug resistance in chemotherapy in OS patients. Taken together, our founding suggested that ALDH1B1 contributes to OS tumor progression and drug resistance, which may represent a novel prognostic marker and potential therapeutic target for OS patients.
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