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高迁移率族蛋白 B1 对结肠炎相关结肠癌黏膜免疫和上皮分化的影响。

Effects of High-Mobility Group Box-1 on Mucosal Immunity and Epithelial Differentiation in Colitic Carcinoma.

机构信息

Department of Molecular Pathology, Nara Medical University, 840 Shijo-Cho, Kashihara 634-8521, Nara, Japan.

Pathology Laboratory, Research Institute, Tokushukai Nozaki Hospital, 2-10-50 Tanigawa, Daito 574-0074, Osaka, Japan.

出版信息

Int J Mol Sci. 2024 Jun 21;25(13):6846. doi: 10.3390/ijms25136846.

DOI:10.3390/ijms25136846
PMID:38999957
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11241214/
Abstract

Abnormalities in mucosal immunity are involved in the onset and progression of ulcerative colitis (UC), resulting in a high incidence of colorectal cancer (CRC). While high-mobility group box-1 (HMGB1) is overexpressed during colorectal carcinogenesis, its role in UC-related carcinogenesis remains unclear. In the present study, we investigated the role of HMGB1 in UC-related carcinogenesis and sporadic CRC. Both the azoxymethane colon carcinogenesis and dextran sulfate sodium colitis carcinogenesis models demonstrated temporal increases in mucosal HMGB1 levels. Activated CD8+ cells initially increased and then decreased, whereas exhausted CD8+ cells increased. Additionally, we observed increased regulatory CD8+ cells, decreased naïve CD8+ cells, and decreased mucosal epithelial differentiation. In the in vitro study, HMGB1 induced energy reprogramming from oxidative phosphorylation to glycolysis in CD8+ cells and intestinal epithelial cells. Furthermore, in UC dysplasia, UC-related CRC, and hyperplastic mucosa surrounding human sporadic CRC, we found increased mucosal HMGB1, decreased activated CD8+ cells, and suppressed mucosal epithelial differentiation. However, we observed increased activated CD8+ cells in active UC mucosa. These findings indicate that HMGB1 plays an important role in modulating mucosal immunity and epithelial dedifferentiation in both UC-related carcinogenesis and sporadic CRC.

摘要

黏膜免疫异常参与溃疡性结肠炎（UC）的发病和进展，导致结直肠癌（CRC）的发病率较高。虽然高迁移率族蛋白 B1（HMGB1）在结直肠癌变过程中过度表达，但它在 UC 相关癌变中的作用尚不清楚。在本研究中，我们研究了 HMGB1 在 UC 相关癌变和散发性 CRC 中的作用。在氧化偶氮甲烷结肠癌变和葡聚糖硫酸钠结肠炎癌变模型中，黏膜 HMGB1 水平均呈现时间性增加。活化的 CD8+细胞最初增加，然后减少，而耗竭的 CD8+细胞增加。此外，我们观察到调节性 CD8+细胞增加，幼稚 CD8+细胞减少，黏膜上皮分化减少。在体外研究中，HMGB1 诱导 CD8+细胞和肠上皮细胞从氧化磷酸化向糖酵解的能量重编程。此外，在 UC 异型增生、UC 相关 CRC 和人散发性 CRC 周围的增生性黏膜中，我们发现黏膜 HMGB1 增加，活化的 CD8+细胞减少，黏膜上皮分化受抑制。然而，在活动性 UC 黏膜中观察到活化的 CD8+细胞增加。这些发现表明 HMGB1 在调节黏膜免疫和上皮去分化方面在 UC 相关癌变和散发性 CRC 中都发挥着重要作用。

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