BACKGROUND: Ameloblastoma is the most common clinically-significant epithelial odontogenic tumor, and is considered a benign but locally-aggressive tumor of the craniofacial region. Osteonectin/secreted protein acidic and rich in cysteine (SPARC) is induced in response to a number of biological processes such as tumor growth and metastasis, whereas matrix metalloproteinases (MMPs) degrade the extracellular matrix and participate in various biological processes including tumor invasion and metastasis. We hypothesize that SPARC acts with MMPs for the local invasiveness of ameloblastoma. The aim of this study was to examine the association of SPARC with MMP-1, MMP-2, and MMP-9 in ameloblastoma. METHOD: Immunohistochemical expression of SPARC, MMP-1, MMP-2, and MMP-9 as well as co-expression of SPARC and MMP-9 were examined in a cohort of 23 cases of ameloblastoma. RESULTS: SPARC, MMP-1, -2, and -9 were detected in the cytoplasm of the ameloblastic-like columnar cells and stellate-reticulum-like cells as well as in the stromal tissues of fibroblasts and endothelial cells of our cohort of ameloblastoma patients. Furthermore, co-expression of SPARC and MMP-9 were found in 23 cases of ameloblastoma. This may be the first study to demonstrate that the expression level of SPARC was statistically correlated with MMP-9 but not with MMP-1 or -2 in ameloblastoma. CONCLUSION: Our results suggest a putative association between SPARC and MMPs (especially MMP-9) in ameloblastoma to regulate tumor invasion.
BACKGROUND:Ameloblastoma is the most common clinically-significant epithelial odontogenic tumor, and is considered a benign but locally-aggressive tumor of the craniofacial region. Osteonectin/secreted protein acidic and rich in cysteine (SPARC) is induced in response to a number of biological processes such as tumor growth and metastasis, whereas matrix metalloproteinases (MMPs) degrade the extracellular matrix and participate in various biological processes including tumor invasion and metastasis. We hypothesize that SPARC acts with MMPs for the local invasiveness of ameloblastoma. The aim of this study was to examine the association of SPARC with MMP-1, MMP-2, and MMP-9 in ameloblastoma. METHOD: Immunohistochemical expression of SPARC, MMP-1, MMP-2, and MMP-9 as well as co-expression of SPARC and MMP-9 were examined in a cohort of 23 cases of ameloblastoma. RESULTS:SPARC, MMP-1, -2, and -9 were detected in the cytoplasm of the ameloblastic-like columnar cells and stellate-reticulum-like cells as well as in the stromal tissues of fibroblasts and endothelial cells of our cohort of ameloblastomapatients. Furthermore, co-expression of SPARC and MMP-9 were found in 23 cases of ameloblastoma. This may be the first study to demonstrate that the expression level of SPARC was statistically correlated with MMP-9 but not with MMP-1 or -2 in ameloblastoma. CONCLUSION: Our results suggest a putative association between SPARC and MMPs (especially MMP-9) in ameloblastoma to regulate tumor invasion.
Authors: Eliane Macedo Sobrinho Santos; Hércules Otacílio Santos; Ivoneth Dos Santos Dias; Sérgio Henrique Santos; Alfredo Maurício Batista de Paula; John David Feltenberger; André Luiz Sena Guimarães; Lucyana Conceição Farias Journal: Int J Mol Cell Med Date: 2016-12-06