The expression of NF-κB, Ki-67 and MMP-9 in CCOT, DGCT and GCOC

被引:26
作者
Gong, Yanling [2 ,3 ]
Wang, Li [1 ,2 ]
Wang, Hengkun [4 ]
Li, Tiejun [5 ]
Chen, Xinming [1 ,2 ]
机构
[1] Wuhan Univ, Sch & Hosp Stomatol, Dept Pathol, Wuhan 430072, Hubei, Peoples R China
[2] Wuhan Univ, Sch & Hosp Stomatol, Minist Educ, Key Lab Oral Biomed Engn, Wuhan 430072, Hubei, Peoples R China
[3] Second Hosp Weihai, Dept Stomatol, Weihai, Shandong, Peoples R China
[4] Weihai Municipal Hosp, Weihai, Shandong, Peoples R China
[5] Peking Univ, Sch & Hosp Stomatol, Dept Pathol, Beijing 100871, Peoples R China
关键词
Calcifying odontogenic cyst; Nuclear factor kappa B; Proliferation; Matrix metalloproteinase; Calcifying cystic odontogenic tumor (CCOT); Dentinogenic ghost cell tumor (DGCT); Ghost cell odontogenic carcinoma (GCOC); MATRIX METALLOPROTEINASES; TUMOR PROGRESSION; SQUAMOUS-CELL; INHIBITORS; CARCINOMA; ALPHA; ADENOCARCINOMA; LOCALIZATION;
D O I
10.1016/j.oraloncology.2008.07.004
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Calcifying odontogenic cysts (COCs) represent a group of rare odontogenic lesions with a diversity of clinicopathological and behavioral features. According to the WHO classification of head and neck tumors in 2005, COC has been divided into calcifying cystic odontogenic tumor (CCOT), dentinogenic ghost cell tumor (DGCT) and ghost cell odontogenic carcinoma (GCOC). With few reports available on its immunohistochemical pro. le, this study investigated the histopathological features and the expression of nuclear factor kappa B (NF-kappa B), Ki-67 and matrix metalloproteinase-9 (MMP-9) in CCOT, DGCT and GCOC. According to the WHO classification of head and neck tumors in 2005, 26 cases of the so-called COC were diagnosed as CCOT (n = 14), DGCT (n = 7) and GCOC (n = 5), respectively. The specimens of 26 COCs and 10 classic ameloblastomas (as control group) were examined by immunohistochemistry using anti-NF-kappa B p65, anti-Ki67 and anti-MMP-9 antibodies and by in situ hybridization (ISH) using anti-MMP-9 mRNA probes. Immunohistochemical reactivity for NF-kappa B was mainly detected in the cytoplasm of tumor cells, and nuclear reactivity was only seen in few tumor cells in COC and classic ameloblastomas. Rate of nuclear staining was less than 1%. The expression of Ki-67 in GCOC was significantly higher than those in CCOT (p < 0.001), DGCT and ameloblastoma (p < 0.005). In COCs and ameloblastomas, expression of MMP-9 mRNA and protein was detected in tumor cells as well as in stromal cells. The positive staining for MMP-9 protein was detected in stromal cells of all GCOC cases and was significantly stronger than those in CCOT and DGCT groups (p < 0.05). NF-kappa B may minimally affect the progression and local invasiveness of CCOT, DGCT and GCOC. GCOC show significantly higher proliferative activity than CCOT and DGCT. MMP-9 in stroma is associated with invasive ability of the CCOT, DGCT and GCOC. (C) 2008 Elsevier Ltd. All rights reserved.
引用
收藏
页码:515 / 520
页数:6
相关论文
共 27 条
[1]  
Bhuvarahamurthy V, 2006, ONCOL REP, V15, P1379
[2]   Ki67 protein: the immaculate deception? [J].
Brown, DC ;
Gatter, KC .
HISTOPATHOLOGY, 2002, 40 (01) :2-11
[3]  
CANETESOLER R, 1994, AM J PATHOL, V144, P518
[4]   Stromal matrix metalloproteinase-9 regulates the vascular architecture in neuroblastoma by promoting pericyte recruitment [J].
Chantrain, CF ;
Shimada, H ;
Jodele, S ;
Groshen, S ;
Ye, W ;
Shalinsky, DR ;
Werb, Z ;
Coussens, LM ;
DeClerck, YA .
CANCER RESEARCH, 2004, 64 (05) :1675-1686
[5]  
GORLIN R J, 1962, Oral Surg Oral Med Oral Pathol, V15, P1235, DOI 10.1016/0030-4220(62)90159-7
[6]   NF-κB promotes breast cancer cell migration and metastasis by inducing the expression of the chemokine receptor CXCR4 [J].
Helbig, G ;
Christopherson, KW ;
Bhat-Nakshatri, P ;
Kumar, S ;
Kishimoto, H ;
Miller, KD ;
Broxmeyer, HE ;
Nakshatri, H .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (24) :21631-21638
[7]   Development of matrix metalloproteinase inhibitors in cancer therapy [J].
Hidalgo, M ;
Eckhardt, SG .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 2001, 93 (03) :178-193
[8]  
HIMELSTEIN BP, 1994, INVAS METAST, V14, P246
[9]  
KADOWAKI T, 1994, CANCER RES, V54, P291
[10]  
KRAMER IRH, 1992, WHO INT HISTOLOGICAL, P20