Limits...
Potential role of S-adenosylmethionine in osteosarcoma development.

Shi H, Mu WD, Zhang B, Meng T, Zhang ST, Zhou DS - Onco Targets Ther (2016)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Traumatic Orthopaedics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan; Department of Bone and Joint Surgery.

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.

No MeSH data available.


Related in: MedlinePlus

Analysis of Sox2 expression in normal and osteosarcoma tissues.Notes: (A) Sox2 expression in normal bone tissue of a mouse. (B) Sox2 expression in primary osteosarcoma tissue. (C) Sox2 expression in metastatic osteosarcoma tissue. (D) Sox2 expression in SAM-treated primary osteosarcoma tissue. (E) Sox2 expression in SAM-treated metastatic osteosarcoma tissue. Scale bar: 100 µm.Abbreviation: SAM, S-adenosylmethionine.
© Copyright Policy
Related In: Results  -  Collection

License 1 - License 2
getmorefigures.php?uid=PMC4920229&req=5

f2-ott-9-3653: Analysis of Sox2 expression in normal and osteosarcoma tissues.Notes: (A) Sox2 expression in normal bone tissue of a mouse. (B) Sox2 expression in primary osteosarcoma tissue. (C) Sox2 expression in metastatic osteosarcoma tissue. (D) Sox2 expression in SAM-treated primary osteosarcoma tissue. (E) Sox2 expression in SAM-treated metastatic osteosarcoma tissue. Scale bar: 100 µm.Abbreviation: SAM, S-adenosylmethionine.

Mentions: The immunohistochemistry of normal bone tissue with anti-Sox2 antibody showed a minimal expression as illustrated in Figure 2A. But in response to osteosarcoma progression, its expression got upregulated (Figure 2B and C). In the case of primary osteosarcoma, patches of cells showed signals for Sox2 (Figure 2B), whereas in the metastatic form of osteosarcoma, strong signals were visualized from the background of higher proliferative mass of cells (Figure 2C). With SAM administration, osteosarcoma tissue showed histological improvement along with the repressed expression of Sox2 protein in the primary stage of osteosarcoma (Figure 2D). Following SAM treatment, the osteosarcoma development was controlled in the primary stage with a minimal expression of Sox2 along with restitution of the cellular arrangement (Figure 2D). But Sox2 expression was not restricted in the advanced stage of metastatic osteosarcoma (Figure 2E).


Potential role of S-adenosylmethionine in osteosarcoma development.

Shi H, Mu WD, Zhang B, Meng T, Zhang ST, Zhou DS - Onco Targets Ther (2016)

Analysis of Sox2 expression in normal and osteosarcoma tissues.Notes: (A) Sox2 expression in normal bone tissue of a mouse. (B) Sox2 expression in primary osteosarcoma tissue. (C) Sox2 expression in metastatic osteosarcoma tissue. (D) Sox2 expression in SAM-treated primary osteosarcoma tissue. (E) Sox2 expression in SAM-treated metastatic osteosarcoma tissue. Scale bar: 100 µm.Abbreviation: SAM, S-adenosylmethionine.
© Copyright Policy
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4920229&req=5

f2-ott-9-3653: Analysis of Sox2 expression in normal and osteosarcoma tissues.Notes: (A) Sox2 expression in normal bone tissue of a mouse. (B) Sox2 expression in primary osteosarcoma tissue. (C) Sox2 expression in metastatic osteosarcoma tissue. (D) Sox2 expression in SAM-treated primary osteosarcoma tissue. (E) Sox2 expression in SAM-treated metastatic osteosarcoma tissue. Scale bar: 100 µm.Abbreviation: SAM, S-adenosylmethionine.
Mentions: The immunohistochemistry of normal bone tissue with anti-Sox2 antibody showed a minimal expression as illustrated in Figure 2A. But in response to osteosarcoma progression, its expression got upregulated (Figure 2B and C). In the case of primary osteosarcoma, patches of cells showed signals for Sox2 (Figure 2B), whereas in the metastatic form of osteosarcoma, strong signals were visualized from the background of higher proliferative mass of cells (Figure 2C). With SAM administration, osteosarcoma tissue showed histological improvement along with the repressed expression of Sox2 protein in the primary stage of osteosarcoma (Figure 2D). Following SAM treatment, the osteosarcoma development was controlled in the primary stage with a minimal expression of Sox2 along with restitution of the cellular arrangement (Figure 2D). But Sox2 expression was not restricted in the advanced stage of metastatic osteosarcoma (Figure 2E).

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Traumatic Orthopaedics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan; Department of Bone and Joint Surgery.

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.

No MeSH data available.


Related in: MedlinePlus