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Abstract：
BACKGROUND: Odontogenic lesions constitute a heterogeneous group of lesions. CLIC4 protein regulates different cellular processes, including epithelial-mesenchymal transition and fibroblast-myofibroblast transdifferentiation. This study analyzed CLIC4, E-cadherin, Vimentin, and α-SMA immunoexpression in epithelial odontogenic lesions that exhibit different biological behavior.
METHODS: It analyzed the immunoexpression of CLIC4, E-cadherin, and Vimentin in the epithelial cells, as well as CLIC4 and α-SMA in the mesenchymal cells, of ameloblastoma (AM) (n = 16), odontogenic keratocyst (OKC) (n = 20), and adenomatoid odontogenic tumor (AOT) (n = 8). Immunoexpressions were categorized as score 0 (0% positive cells), 1 (< 25%), 2 (≥ 25% - < 50%), 3 (≥ 50% - < 75%), or 4 (≥ 75%).
RESULTS: Cytoplasmic CLIC4 immunoexpression was higher in AM and AOT (p < 0.001) epithelial cells. Nuclear-cytoplasmic CLIC4 was higher in OKC\'s epithelial lining (p < 0.001). Membrane (p = 0.012) and membrane-cytoplasmic (p < 0.001) E-cadherin immunoexpression were higher in OKC, while cytoplasmic E-cadherin expression was higher in AM and AOT (p < 0.001). Vimentin immunoexpression was higher in AM and AOT (p < 0.001). Stromal CLIC4 was higher in AM and OKC (p = 0.008). Similarly, α-SMA immunoexpression was higher in AM and OKC (p = 0.037). Correlations in these proteins\' immunoexpression were observed in AM and OKC (p < 0.05).
CONCLUSIONS: CLIC4 seems to regulate the epithelial-mesenchymal transition, modifying E-cadherin and Vimentin expression. In mesenchymal cells, CLIC4 may play a role in fibroblast-myofibroblast transdifferentiation. CLIC4 may be associated with epithelial odontogenic lesions with aggressive biological behavior.
METHODS: It analyzed the immunoexpression of CLIC4, E-cadherin, and Vimentin in the epithelial cells, as well as CLIC4 and α-SMA in the mesenchymal cells, of ameloblastoma (AM) (n = 16), odontogenic keratocyst (OKC) (n = 20), and adenomatoid odontogenic tumor (AOT) (n = 8). Immunoexpressions were categorized as score 0 (0% positive cells), 1 (< 25%), 2 (≥ 25% - < 50%), 3 (≥ 50% - < 75%), or 4 (≥ 75%).
RESULTS: Cytoplasmic CLIC4 immunoexpression was higher in AM and AOT (p < 0.001) epithelial cells. Nuclear-cytoplasmic CLIC4 was higher in OKC\'s epithelial lining (p < 0.001). Membrane (p = 0.012) and membrane-cytoplasmic (p < 0.001) E-cadherin immunoexpression were higher in OKC, while cytoplasmic E-cadherin expression was higher in AM and AOT (p < 0.001). Vimentin immunoexpression was higher in AM and AOT (p < 0.001). Stromal CLIC4 was higher in AM and OKC (p = 0.008). Similarly, α-SMA immunoexpression was higher in AM and OKC (p = 0.037). Correlations in these proteins\' immunoexpression were observed in AM and OKC (p < 0.05).
CONCLUSIONS: CLIC4 seems to regulate the epithelial-mesenchymal transition, modifying E-cadherin and Vimentin expression. In mesenchymal cells, CLIC4 may play a role in fibroblast-myofibroblast transdifferentiation. CLIC4 may be associated with epithelial odontogenic lesions with aggressive biological behavior.
摘要：
背景：牙源性病变构成一组异质性病变。CLIC4蛋白调节不同的细胞过程，包括上皮-间质转化和成纤维细胞-肌成纤维细胞转分化。这项研究分析了CLIC4，E-钙黏着蛋白，Vimentin,和α-SMA在表现出不同生物学行为的上皮牙源性病变中的免疫表达。
方法：分析CLIC4、E-cadherin、和上皮细胞中的波形蛋白，以及间充质细胞中的CLIC4和α-SMA，成釉细胞瘤（AM）（n=16），牙源性角化囊肿（OKC）（n=20），和腺瘤样牙源性肿瘤（AOT）（n=8）。免疫表达分为0分（0％阳性细胞），1（<25%），2（≥25%-<50%），3（≥50%-<75%），或4（≥75%）。
结果：细胞质CLIC4免疫表达在AM和AOT上皮细胞中更高（p<0.001）。核质CLIC4在OKC的上皮衬里中更高（p<0.001）。OKC中膜(p=0.012)和膜-细胞质(p<0.001)E-cadherin免疫表达较高,而AM和AOT的细胞质E-cadherin表达较高(p<0.001)。波形蛋白在AM和AOT中的免疫表达较高(p<0.001)。基质CLIC4在AM和OKC中较高(p=0.008)。同样，α-SMA在AM和OKC中的免疫表达较高(p=0.037)。在AM和OKC中观察到这些蛋白质免疫表达的相关性(p<0.05)。
结论：CLIC4似乎调节上皮-间质转化，改变E-cadherin和波形蛋白的表达。在间充质细胞中，CLIC4可能在成纤维细胞-肌成纤维细胞转分化中起作用。CLIC4可能与具有侵袭性生物学行为的上皮牙源性病变有关。
方法：分析CLIC4、E-cadherin、和上皮细胞中的波形蛋白，以及间充质细胞中的CLIC4和α-SMA，成釉细胞瘤（AM）（n=16），牙源性角化囊肿（OKC）（n=20），和腺瘤样牙源性肿瘤（AOT）（n=8）。免疫表达分为0分（0％阳性细胞），1（<25%），2（≥25%-<50%），3（≥50%-<75%），或4（≥75%）。
结果：细胞质CLIC4免疫表达在AM和AOT上皮细胞中更高（p<0.001）。核质CLIC4在OKC的上皮衬里中更高（p<0.001）。OKC中膜(p=0.012)和膜-细胞质(p<0.001)E-cadherin免疫表达较高,而AM和AOT的细胞质E-cadherin表达较高(p<0.001)。波形蛋白在AM和AOT中的免疫表达较高(p<0.001)。基质CLIC4在AM和OKC中较高(p=0.008)。同样，α-SMA在AM和OKC中的免疫表达较高(p=0.037)。在AM和OKC中观察到这些蛋白质免疫表达的相关性(p<0.05)。
结论：CLIC4似乎调节上皮-间质转化，改变E-cadherin和波形蛋白的表达。在间充质细胞中，CLIC4可能在成纤维细胞-肌成纤维细胞转分化中起作用。CLIC4可能与具有侵袭性生物学行为的上皮牙源性病变有关。
