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基质金属蛋白酶、金属蛋白酶组织抑制剂和生长因子调节牙源性角化囊性瘤的侵袭性和增殖活性。

Matrix metalloproteinases, tissue inhibitors of metalloproteinases, and growth factors regulate the aggressiveness and proliferative activity of keratocystic odontogenic tumors.

机构信息

Department of Oral and Maxillofacial Surgery, School of Dentistry, University Center of Pará, Belém, Brazil.

出版信息

Oral Surg Oral Med Oral Pathol Oral Radiol. 2012 Oct;114(4):487-96. doi: 10.1016/j.oooo.2012.06.011.

Abstract

OBJECTIVE

The objective of this preliminary study was to evaluate the expression of matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs) and growth factors in keratocystic odontogenic tumors (KOTs).

STUDY DESIGN

The expression of MMPs, TIMPs, growth factors, and the extracellular signal-regulated kinase (ERK) 1/2 signaling pathway were assessed by immunohistochemistry in 15 cases of KOT and 4 cases of calcifying cystic odontogenic tumor (CCOT).

RESULTS

KOT samples expressed significantly higher amounts of MMPs, TIMPs, growth factors, epidermal growth factor receptor (EGFR), and ERK compared with CCOT samples, with the exception of MMP-2 and TIMP-1.

CONCLUSIONS

MMP-9, TIMP-2, EGF and transforming growth factor α act together and likely regulate the proliferation and aggressiveness of KOT. ERK-1/2 serves as the transducer of signals generated by these proteins, which signal through the common receptor, EGFR. This process may be related to the increased proliferation and aggressiveness observed in KOT.

摘要

目的

本初步研究旨在评估基质金属蛋白酶(MMPs)、金属蛋白酶组织抑制剂(TIMPs)和生长因子在牙源性角化囊性瘤(KOTs)中的表达。

研究设计

通过免疫组织化学方法评估了 15 例 KOT 和 4 例牙源性钙化囊性瘤(CCOT)中 MMPs、TIMP、生长因子和细胞外信号调节激酶(ERK)1/2 信号通路的表达。

结果

与 CCOT 样本相比,KOT 样本表达的 MMPs、TIMP、生长因子、表皮生长因子受体(EGFR)和 ERK 明显更高,除 MMP-2 和 TIMP-1 外。

结论

MMP-9、TIMP-2、EGF 和转化生长因子 α 共同作用,可能调节 KOT 的增殖和侵袭性。ERK-1/2 作为这些蛋白产生的信号转导子,通过共同受体 EGFR 传递信号。这一过程可能与 KOT 中观察到的增殖和侵袭性增加有关。

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