IL-6/JAK2/STAT3通路介导牙龈二氧化碳嗜纤维菌促进口腔鳞癌细胞迁移与侵袭

doi:10.13591/j.cnki.kqyx.2026.09.005

摘要/Abstract

摘要：

目的本研究旨在探讨白细胞介素-6(interleukin-6, IL-6)/蛋白酪氨酸激酶2(Janus kinase 2, JAK2)/信号转导和转录激活因子3(signal transducer and activator of transcription 3, STAT3)通路介导下牙龈二氧化碳嗜纤维菌(Capnocytophaga gingivalis,C. gingivalis)对口腔鳞癌(oral squamous cell carcinoma, OSCC)细胞迁移与侵袭的促进作用。方法将SCC9细胞与裸鼠分别分为Control组、C. gingivalis组和C. gingivalis+AG490组。采用CCK-8法检测各组细胞活力,Transwell检测各组细胞迁移与侵袭能力,检测各组裸鼠体内致瘤能力,HE染色检测各组裸鼠组织病理变化,Western blot检测各组细胞及组织上皮间充质转化(epithelial-mesenchymal transition, EMT)标志蛋白E-cadherin、N-cadherin、Vimentin和IL-6、p-JAK2/JAK2、p-STAT3/STAT3的水平。结果体内外实验均显示,与Control组相比,C. gingivalis组E-cadherin蛋白水平降低,N-cadherin、Vimentin蛋白、IL-6、p-JAK2/JAK2、p-STAT3/STAT3水平均升高;与C. gingivalis组相比,C. gingivalis+AG490组E-cadherin蛋白水平升高,其余蛋白水平均降低(均P<0.05)。体外实验显示,与Control组相比,C. gingivalis组细胞增殖能力显著升高,迁移与侵袭细胞数目增多;与C. gingivalis组相比,C. gingivalis+AG490组增殖能力显著降低,迁移与侵袭细胞数目减少(均P<0.05)。体内实验显示,与Control组相比,C. gingivalis组裸鼠的肿瘤体积与质量均显著增加,HE染色显示移植瘤组织出现明显的增生与癌变;与C. gingivalis组相比,C. gingivalis+AG490组裸鼠的肿瘤体积与质量均显著降低,HE染色显示移植瘤组织癌变减轻(均P<0.05)。结论 C. gingivalis通过激活IL-6/JAK2/STAT3信号通路促进OSCC细胞迁移与侵袭。

关键词: 口腔鳞状细胞癌, 白细胞介素-6, 牙龈二氧化碳嗜纤维菌, 蛋白酪氨酸激酶2, 信号转导和转录激活因子3

Abstract:

Objective To investigate the promotion of the migration and invasion of oral squamous cell carcinoma (OSCC) cells by Capnocytophaga gingivalis(C. gingivalis) mediated by the interleukin-6(IL-6)/Janus kinase 2(JAK2)/signal transducer and activator of transcription 3(STAT3) pathway. Methods SCC9 cells and nude mice were divided into the Control group, C. gingivalis group, and C. gingivalis+AG490 group. The CCK-8 method was used to detect cell viability in each group. Transwell assay was employed to determine the migration and invasion abilities of cells in each group. The tumorigenic ability in nude mice of each group was detected. HE staining was used to examine the histopathological changes in nude mouse tissues of each group, and Western blot was applied to detect the levels of epithelial-mesenchymal transition(EMT) marker proteins(E-cadherin, N-cadherin, Vimentin) as well as IL-6, p-JAK2/JAK2, p-STAT3/STAT3 in cells and tissues of each group. Results Both in vitro and in vivo experiments showed that compared with the Control group, the protein level of E-cadherin in the C. gingivalis group decreased, while the protein levels of N-cadherin, Vimentin, IL-6, p-JAK2/JAK2, p-STAT3/STAT3 increased. Compared with the C. gingivalis group, the protein level of E-cadherin in the C. gingivalis+AG490 group increased, and the levels of the remaining proteins decreased(all P<0.05). In vitro experiments showed that compared with the Control group, the cell proliferation ability in the C. gingivalis group was increased significantly, and the number of migrative and invasive cells increased. Compared with the C. gingivalis group, the cell proliferation ability of the C. gingivalis+AG490 group decreased significantly, and the number of migrative and invasive cells decreased(all P<0.05). In vivo experiments showed that compared with the Control group, the tumor volume and weight of nude mice in the C. gingivalis group increased significantly, and HE staining showed that obvious hyperplasia and carcinogenesis occurred in the transplanted tumor tissue. Compared with the C. gingivalis group, the tumor volume and weight of nude mice in the C. gingivalis+AG490 group decreased significantly, and HE staining showed that carcinogenesis of the transplanted tumor tissue was alleviated(all P<0.05). Conclusion C. gingivalis promotes the migration and invasion of OSCC cells by activating the IL-6/JAK2/STAT3 signaling pathway.

Key words: oral squamous cell carcinoma, interleukin-6, Capnocytophaga gingivalis, Janus kinase 2, signal transducer and activator of transcription 3

中图分类号:

R739.8

王钧正, 段博文, 胥晓萍, 周建华, 董刚. IL-6/JAK2/STAT3通路介导牙龈二氧化碳嗜纤维菌促进口腔鳞癌细胞迁移与侵袭[J]. 口腔医学, 2026, 46(9): 671-676.

WANG Junzheng, DUAN Bowen, XU Xiaoping, ZHOU Jianhua, DONG Gang. Capnocytophaga gingivalis promotes the migration and invasion of oral squamous cell carcinoma cells mediated by the IL-6/JAK2/STAT3 pathway[J]. Stomatology, 2026, 46(9): 671-676.

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