成纤维细胞调节综合征性角化囊性瘤和非综合征性牙源性肿瘤的可变侵袭性。
Fibroblasts regulate variable aggressiveness of syndromic keratocystic and non-syndromic odontogenic tumors.
机构信息
Department of Oral Pathology, Peking University School and Hospital of Stomatology, 22 Zhongguancun Avenue South, Haidian District, Beijing 100081, China.
Central Laboratory, Peking University School and Hospital of Stomatology, 22 Zhongguancun Avenue South, Haidian District, Beijing 100081, China
出版信息
J Dent Res. 2014 Sep;93(9):904-10. doi: 10.1177/0022034514542108. Epub 2014 Jun 27.
UNLABELLED
Keratocystic odontogenic tumors (KCOTs) are jaw lesions that can be either sporadic or associated with nevoid basal cell carcinoma syndrome, which typically occurs as multiple, aggressive lesions that can lead to large areas of bone destruction and resorption and cause major impairment and even jaw fracture. To clarify the role of fibroblasts in the aggressivness of syndromic (S-) as compared with non-syndromic (NS-) KCOTs, we assessed fibroblasts derived from 16 S- and NS-KCOTs for differences in cell proliferation, multilineage differentiation potential, alkaline phosphatase activity, and osteoclastogenic potential. S-KCOT fibroblasts had proliferative and osteoclastogenic capacity higher than those from NS-KCOTs, as evidenced by higher numbers of tartrate-resistant acid-phosphatase-positive multinuclear cells, expression of cyclooxygenase 2, and ratio of receptor activator of nuclear factor-kappa B ligand to osteoprotegerin. The osteogenic potential was higher for S- than for NS-KCOT fibroblasts and was associated with lower mRNA expression of runt-related transcription factor 2, collagen type I α1, osteocalcin, and osteopontin as well as reduced alkaline phosphatase activity. These results suggest that the distinct characteristics of fibroblasts in KCOTs are responsible for the greater aggressiveness observed in the syndromic subtype.
ABBREVIATIONS
AP, alkaline phosphatase; CK, cytokeratin; COL1A1, collagen type I α1; COX-2, cyclooxygenase-2; GM-CSF, granulocyte-macrophage colony-stimulating factor; IL-1α, interleukin 1α; KCOT, keratocystic odontogenic tumor; NBCCS, nevoid basal cell carcinoma syndrome; NS-KCOT, non-syndrome-associated KCOT; OCN, osteocalcin; OPG, osteoprotegerin; OPN, osteopontin; RANKL, receptor activator of nuclear factor-kappa B ligand; Runx2, runt-related transcription factor 2; S-KCOT, syndrome-associated KCOT; TAF, tumor-associated fibroblast; and TRAP, tartrate-resistant acid phosphatase.
未加标签
牙源性角化囊性瘤（KCOTs）是一种颌骨病变，可以是散发性的，也可以与基底细胞痣综合征相关联，基底细胞痣综合征通常表现为多发性、侵袭性病变，可导致大面积骨破坏和吸收，并导致严重的损伤，甚至颌骨骨折。为了阐明纤维母细胞在综合征（S-）KCOT 与非综合征（NS-）KCOT 的侵袭性中的作用，我们评估了来自 16 个 S-和 NS-KCOT 的纤维母细胞在细胞增殖、多谱系分化潜能、碱性磷酸酶活性和破骨细胞生成潜能方面的差异。S-KCOT 纤维母细胞的增殖和破骨细胞生成能力高于 NS-KCOT 纤维母细胞，这表现在抗酒石酸酸性磷酸酶阳性多核细胞数量较多、环氧化酶 2 的表达以及核因子-kappa B 配体受体激活物与护骨素的比值较高。S-KCOT 纤维母细胞的成骨潜能高于 NS-KCOT 纤维母细胞，并且与 runt 相关转录因子 2、I 型胶原α1、骨钙素和骨桥蛋白的 mRNA 表达降低以及碱性磷酸酶活性降低有关。这些结果表明，KCOT 中纤维母细胞的独特特征是导致综合征型亚型观察到的更大侵袭性的原因。
缩写词
AP，碱性磷酸酶；CK，细胞角蛋白；COL1A1，I 型胶原α1；COX-2，环氧化酶-2；GM-CSF，粒细胞-巨噬细胞集落刺激因子；IL-1α，白细胞介素 1α；KCOT，牙源性角化囊性瘤；NBCCS，基底细胞痣综合征；NS-KCOT，非综合征相关 KCOT；OCN，骨钙素；OPG，护骨素；OPN，骨桥蛋白；RANKL，核因子-kappa B 配体受体激活物；Runx2， runt 相关转录因子 2；S-KCOT，综合征相关 KCOT；TAF，肿瘤相关纤维母细胞；和 TRAP，抗酒石酸酸性磷酸酶。
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