Department of General Dentistry, The Ninth People's Hospital Affiliated to Shanghai JiaoTong University School of Medicine, Shanghai 200000, P.R. China.
Department of Stomatology, Tai'an Central Hospital, Tai'an, Shandong 271000, P.R. China.
Oncol Rep. 2018 Apr;39(4):1793-1804. doi: 10.3892/or.2018.6251. Epub 2018 Feb 7.
Oral leukoplakia (OL) is one of the most common oral precancerous lesions with the possibility of malignant transformation, ranging from 17 to 24% of patients with a median follow-up of >7 years. Previous research has revealed that compared with normal oral epithelial tissues, the expression of secretory leukocyte peptidase inhibitor (SLPI) protein is significantly reduced in oral squamous cell carcinoma (OSCC). Based on the above-mentioned research, it is known that SLPI is a potential predictive and diagnostic tool for the progression of oral carcinogenesis. Therefore, we investigated the correlation between the abundance of SLPI protein and the different histological grades of OL by immunohistochemistry. The results indicated that the level of SLPI was negatively correlated with the histological grades of the oral premalignant lesions, indicating that it may be a potential predictive tool for the malignant transformation presented in oral precancerous patients. Subsequently, we investigated the biological effects of SLPI using Cell Counting Kit (CCK)-8, Annexin V/PI apoptosis assay and Caspase-Glo® 3/7 assay. The findings revealed that SLPI promoted apoptosis in the Leuk1 and WSU-HN4 cell lines. Mechanistic studies indicated that SLPI, at least in part, regulated cell apoptosis by inhibiting the expression of TNF receptor-associated factor 1 (TRAF1), which has a close relationship with the nuclear factor-κB (NF-κB) pathway.
口腔白斑病（OL）是最常见的口腔癌前病变之一，有 17%至 24%的患者存在恶性转化的可能，中位随访时间>7 年。先前的研究表明，与正常口腔上皮组织相比，口腔鳞状细胞癌（OSCC）中分泌白细胞蛋白酶抑制剂（SLPI）蛋白的表达显著降低。基于上述研究，已知 SLPI 是口腔癌发生进展的潜在预测和诊断工具。因此，我们通过免疫组织化学研究了 SLPI 蛋白丰度与 OL 不同组织学分级之间的相关性。结果表明，SLPI 水平与口腔癌前病变的组织学分级呈负相关，表明其可能是口腔癌前患者恶性转化的潜在预测工具。随后，我们使用细胞计数试剂盒（CCK）-8、Annexin V/PI 凋亡测定和 Caspase-Glo®3/7 测定研究了 SLPI 的生物学效应。结果表明，SLPI 促进了 Leuk1 和 WSU-HN4 细胞系的凋亡。机制研究表明，SLPI 至少部分通过抑制肿瘤坏死因子受体相关因子 1（TRAF1）的表达来调节细胞凋亡，而 TRAF1 与核因子-κB（NF-κB）途径密切相关。
