Potential role of S-adenosylmethionine in osteosarcoma development

Abstract

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

Keywords

• TCTP
• S-Adenosylmethionine
• K7M2 cells
• Sox2
• BALB/c mouse.