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Potential role of S-adenosylmethionine in osteosarcoma development

Authors Shi H, Mu W, Zhang B, Meng T, Zhang S, Zhou D

Received 27 November 2015

Accepted for publication 10 February 2016

Published 20 June 2016 Volume 2016:9 Pages 3653—3659


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Dekuang Zhao

Peer reviewer comments 3

Editor who approved publication: Dr William Cho

Hui Shi,1,2,* Wei-dong Mu,1,* Bing Zhang,3 Tao Meng,2 Shou-tao Zhang,2 Dong-sheng Zhou1

1Department of Traumatic Orthopaedics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, 2Department of Bone and Joint Surgery, 3Department of Urology Surgery, Binzhou Medical University Hospital, Binzhou, Shandong, People’s Republic of China

*These authors contributed equally to this work

Abstract: The metastatic form of osteosarcoma is a life threatening one since it metastasizes to the lungs. The major cause of metastatic osteosarcoma is hypomethylation of numerous genes that undergo overexpression to enable the progression of the disease. In the present study, S-adenosylmethionine (SAM), a predominant methyl donor, was administered to find out its effects on osteosarcoma progression. As evidence of tumor suppression, the SAM-treated mouse tissue was analyzed histologically, which exemplifies the control that SAM has over abnormal cell proliferation, especially on primary osteosarcoma, but it lacks positive effects on metastatic osteosarcoma. At the molecular level, the successful inhibition of primary osteosarcoma was found to be associated with a lower expression of Sox2, a protein highly expressed in osteosarcoma stem cells, along with an upregulated expression of TCTP. The data suggest that the administration of SAM has a positive role in treating primary osteosarcoma, but it has no role in suppressing metastatic osteosarcoma. The decreased expression of Sox2 together with upregulation of TCTP following SAM administration indicates that SAM has a control over primary osteosarcoma.

Keywords: TCTP, S-adenosylmethionine, K7M2 cells, Sox2, BALB/c mouse

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