Matrix metalloproteinases, TIMPs and growth factors regulating ameloblastoma behaviour

Siqueira, Adriane Sousa de; Carvalho, Márcia Regina; Monteiro, Ana C D; Freitas, Vanessa M.; Jaeger, Ruy Gastaldoni; Pinheiro, João de Jesus Viana

doi:10.1111/j.1365-2559.2010.03596.x

Cited by 51 publications

(58 citation statements)

References 33 publications

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“…Aberrant MMP activity in tumor cells and surrounding stromal tissues has been implicated in tumor invasion and metastasis. According to studies on in vitro and in vivo tumor invasiveness, therapeutic interventions that inhibit MMP activity appear to be very promising [16]. In the present study, no difference was observed in the expression of MMP-9 between ameloblastoma and AOT.…”

Section: Discussioncontrasting

confidence: 44%

Comparação da imunoexpressão de VEGF, TGF-β e MMP-9 em ameloblastoma e tumor odontogênico adenomatóide

Ferreira

Lima

Maia

et al. 2015

Rev. Odonto Ciênc. (Online)

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Purpose: Studies on odontogenic tumors have identified various molecular dysfunctions involved on their development, and some mechanisms such as angiogenesis and matrix modulation, are useful means of investigating the differences in biologic behavior of these tumors. Some important markers to identify tumor aggressiveness by immunohistochemistry are VEGF, TGF-β and MMP-9 proteins. This study aimed to compare the immunohistochemical expression of VEGF, TGF-β, and MMP-9 in ameloblastoma and adenomatoid odontogenic tumor (AOT). Methods: Immunoexpression of VEGF, TGF-β, and MMP-9 was studied in 15 solid ameloblastomas, and 15 AOTs. A semi-quantitative analysis of the immunostained cells was performed, and the statistical analysis was made using the Mann-Whitney nonparametric and Spearman correlation test, with significance level at .05 (P<.05). Results: A higher epithelial immunoexpression of VEGF and TGF-β was observed in ameloblastoma and AOT, respectively, and the stromal reactivity to VEGF was statistically higher in ameloblastoma (P<.05). No statistical difference was observed for MMP-9 (P>.05). Conclusion:The results suggest the involvement of angiogenesis in tumor progression of ameloblastomas, and the inductive effect of stromal cells in AOT, hence justifying its lower growth potential.

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Section: Discussioncontrasting

confidence: 44%

Comparação da imunoexpressão de VEGF, TGF-β e MMP-9 em ameloblastoma e tumor odontogênico adenomatóide

Ferreira

Lima

Maia

et al. 2015

Rev. Odonto Ciênc. (Online)

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“…Similarly, the staining percentage was less pronounced in the epithelial and stromal components of ameloblastoma compared with the other lesions, a finding suggesting higher production of MMP-9, increased BM degradation and the consequent higher invasion potential of this tumor. Siqueira et al 32 observed intense and diffuse TIMP-2 staining in ameloblastomas, which was associated with lower aggressiveness of the tumor. In an in vitro study, Wang et al 5 showed that overexpression of TIMP-2 in ameloblastoma cells was associated with the suppression of MMP-2 activity and a consequently lower invasion potential.…”

Section: Discussionmentioning

confidence: 97%

Comparative analysis of the immunohistochemical expression of collagen IV, MMP-9, and TIMP-2 in odontogenic cysts and tumors

Henriques

Vasconcelos

Galvão

et al. 2011

Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, an

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Objective. The aim of this study was to evaluate the immunohistochemical expression of collagen IV, matrix metalloproteinase (MMP) 9 and tissue inhibitor of MMP (TIMP) 2 in dentigerous cysts (DCs), radicular cysts (RCs), keratocystic odontogenic tumors (KOTs), and ameloblastomas. Study design. Twenty cases of DCs, 20 RCs, 20 KOTs, and 20 ameloblastomas were selected and analyzed by immunohistochemistry. Results. Most DCs and RCs showed continuous and Ͼ50% staining for collagen IV in the basement membrane of the epithelium, whereas predominantly discontinuous thin and Յ50% staining was observed in KOTs and ameloblastomas, with a significant difference in staining percentage (P Ͻ .001). MMP-9 was diffusely distributed and localized in both epithelial and mesenchymal cells of all of the lesions analyzed. The staining percentage was higher in the epithelium (P ϭ .058) and mesenchyme (P ϭ .005) of KOTs and ameloblastomas. Moreover, the distribution pattern, location, and percentage of expression of TIMP-2 were similar in the lesions studied, except for ameloblastoma, with a significant difference in staining percentage (P Ͻ .001).Conclusion. These results demonstrate that the interaction between collagen IV, MMP-9, and TIMP-2 is an important factor for the establishment of differences in the biologic behavior of the odontogenic cysts and tumors studied. Factors related to the epithelial and mesenchymal components participate in the regulation of the growth of odontogenic cystic lesions and tumors. 1 The altered expression of specific proteins of the extracellular matrix (ECM), associated with the exuberant presence of matrix metalloproteinases (MMPs) and the absence of expression of metalloproteinase inhibitors (TIMPs), may influence the behavior of these lesions. In the case of tumors, this situation contributes to the growth and higher aggressiveness of the tumor. 2 The odontogenic keratocyst, recently reclassified as keratocystic odontogenic tumor (KOT), 3 is known for its aggressive nature and high rate of recurrence, especially compared with other odontogenic cysts. 4 Ameloblastoma is a locally aggressive benign epithelial odontogenic tumor with a marked invasion potential that results in multiple recurrences after enucleation and curettage. 5 In contrast, dentigerous (DC) and radicular (RC) cysts show an indolent behavior and rarely recur after surgical removal. KOT presents a cystic structure similar to that of DC and RC, but its invasive and destructive growth is similar to that of ameloblastoma. 6 KOT, ameloblastoma, DC, and RC show distinct evolutions and biologic behaviors. In view of this fact, a growing number of studies have tried to identify

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“…MMP-9 is known for mediating degradation of basement membrane and remodeling of ECM. Studies have provided compelling evidence that MMP-9 is involved in tumor growth and bone metastases [8,[12][13][14][17][18][19][20][21]. According to Vicente et al [17] MMP-2 and MMP-9 are involved in angiogenesis and tumor growth, suggesting an association of the gelatinases with aggressive behavior and unpredictable clinical course in some human neoplasms.…”

Section: Discussionmentioning

confidence: 99%

“…MMP-9 is also considered to have an important role in bone resorption and is closely related with several osteodestructive pathologies. [8,20,21]. MMP-9 act not only as solubilizers of bone matrix but also as regulators of the initiation of bone resorption [8].…”

Section: Discussionmentioning

confidence: 99%

“…Study has shown that MMP-9 is produced by osteoclast in the human bone tissues and suggest that it can degrade bone collagens in concert with MMP-1 and cysteine proteinases in the subosteoclastic microenvironment [16]. Several studies have been conducted to analyze the MMP-9 expression in ameloblastoma [8,[12][13][14][20][21][22]. MMP-9 expression in ameloblastoma is higher than in other odontogenic cysts and keratocyst odontogenic tumor (KOT).…”

Section: Discussionmentioning

confidence: 99%

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Matrix Metalloproteinase-9 (MMP-9) Expression in Different Subtypes of Ameloblastoma

Anne

Krisnuhoni

Chotimah

et al. 2013

J. Maxillofac. Oral Surg.

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Background Ameloblastoma is a common benign odontogenic tumor of the jaw with a local invasive and highly destructive behavior and can develop in any age, with peak prevalence in 3rd-4th decade. Ameloblastoma can be divided into six histological types: follicular, plexiform, acanthomatous, desmoplastic, granular, and basal cell. Matrix metalloproteinase-9 (MMP-9) (92-kD gelatinase/ type IV collagenases = gelatinase B) is involved in bone resorption by degradation of extracellular matrix and osteoclasts recruitment. Recent studies have found that MMP-9 is expressed by ameloblastoma and has a role in ameloblastoma local invasiveness. Objective To analyze MMP-9 expression between different histological types of ameloblastoma. Material and Method Forty samples of ameloblastoma were collected through consecutive sampling and the MMP-9 expression was detected using immunohistochemistry. Result All samples showed positive MMP-9 expression with moderate to strong intensity. 82.4 % plexiform type and 83.3 % mixed type have strong immunoexpression, significantly different with follicular type with only 36.4 % (P \ 0.05). Conclusion Ameloblastoma plexiform and mixed type have higher MMP-9 expression than ameloblastoma follicular type. Different MMP-9 expression may contribute in different ameloblastoma biological behavior.

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Matrix metalloproteinases, TIMPs and growth factors regulating ameloblastoma behaviour

Abstract: These results suggest an interplay involving growth factors MMPs and TIMPs that may contribute to ameloblastoma behaviour. Signals generated by this molecular network would be transduced by ERK 1/2 pathway.

Cited by 51 publications

References 33 publications

Comparação da imunoexpressão de VEGF, TGF-β e MMP-9 em ameloblastoma e tumor odontogênico adenomatóide

Comparação da imunoexpressão de VEGF, TGF-β e MMP-9 em ameloblastoma e tumor odontogênico adenomatóide

Comparative analysis of the immunohistochemical expression of collagen IV, MMP-9, and TIMP-2 in odontogenic cysts and tumors

Matrix Metalloproteinase-9 (MMP-9) Expression in Different Subtypes of Ameloblastoma

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