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Matrix metalloproteinases, TIMPs and growth factors regulating ameloblastoma behaviour
Author(s) -
Siqueira Adriane S,
Carvalho Marcia R D,
Monteiro Ana C D,
Freitas Vanessa M,
Jaeger Ruy G,
Pinheiro Joao J V
Publication year - 2010
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/j.1365-2559.2010.03596.x
Subject(s) - ameloblastoma , matrix metalloproteinase , pathology , epidermal growth factor , immunohistochemistry , transforming growth factor , growth factor , epidermal growth factor receptor , stroma , cancer research , odontogenic tumor , biology , medicine , receptor , endocrinology , odontogenic , anatomy , maxilla
Siqueira A S, Carvalho M R D, Monteiro A C D, Freitas V M, Jaeger R G & Pinheiro J J V.
(2010) Histopathology 57 , 128–137
Matrix metalloproteinases, TIMPs and growth factors regulating ameloblastoma behaviour Aims: Ameloblastoma is an odontogenic neoplasm with local invasiveness and recurrence. We have previously suggested that growth factors and matrix metalloproteinases (MMPs) influence ameloblastoma invasiveness 1 . The aim was to study expression of MMPs, tissue inhibitor of metalloproteinases (TIMPs) and growth factors in ameloblastoma. Methods and results: Thirteen cases of solid/multicystic ameloblastoma were examined. As a control, calcifying cystic odontogenic tumour (CCOT), a non‐invasive odontogenic neoplasm with ameloblastomatous epithelium was also studied. Immunohistochemistry detected MMPs, TIMPs and growth factors in ameloblastoma and CCOT. The labelling index (LI) of MMP‐9 and TIMP‐2 was significantly higher in ameloblastoma compared with CCOT. The LI of epidermal growth factor (EGF), transforming growth factor (TGF)‐α and epidermal growth factor receptor (EGFR) was also increased in ameloblastoma. This neoplasm showed greater expression of MMPs, TIMPs and growth factors compared with CCOT. We then analysed these molecules in ameloblastoma cells and stroma. Ameloblastoma cells exhibited increased LI of MMP‐1, ‐2 and EGFR. We found a positive correlation between EGF and TIMP‐1, and between TGF‐α and TIMP‐2. It is known that signals generated by growth factors are transduced by the ERK pathway. Ameloblastoma stroma exhibited the phosphorylated (activated) form of ERK. Conclusions: 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.