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氯离子细胞内通道 2 可作为头颈部鳞状细胞癌的恶性因子发挥作用

英文原题:Chloride Intracellular Channel 2 Can Function as a Malignant Factor in Head and Neck Squamous Cell Carcinoma.

查看英文原题

Chloride Intracellular Channel 2 Can Function as a Malignant Factor in Head and Neck Squamous Cell Carcinoma.

PubMed 2025/12/12(内容时间) Head Neck Q1 · IF 2.2(JCR 2025)

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研究概要

CLIC2 可能作为 HNSCC 的一种新型风险因素。

研究思路结论见上方概要

氯离子细胞内通道2(CLIC2)与肿瘤的关联尚不明确。然而,近期研究发现CLIC2在某些肿瘤中表现出抗肿瘤特性。本研究旨在评估CLIC2表达在头颈部鳞状细胞癌(HNSCC)中的临床相关性,以确定其是否发挥与脑肿瘤中相似的抗肿瘤作用,并探索其作为HNSCC新型治疗靶点的潜力。

我们通过细胞生物学分析探索了CLIC在HNSCC中的意义,并研究了CLIC2强制表达的HNSCC细胞系的基因表达谱。通过组织病理学检查了人HNSCC中CLIC2的表达。

在HNSCC细胞中强制表达CLIC2伴随着细胞增殖增加、对NK 细胞的抵抗以及促肿瘤基因的表达,此外在小鼠模型中进行异种移植后致瘤性也增加。在几个人类HNSCC病例中观察到了CLIC2的表达。

展开英文摘要原文

The association of chloride intracellular channel 2 (CLIC2) with tumors has remained unclear. However, recently, CLIC2 was found to exhibit antitumor properties in some tumors. In this study, we aimed to evaluate the clinical relevance of CLIC2 expression in head and neck squamous cell carcinoma (HNSCC) to determine whether it exerts antitumor effects similar to those in brain tumors and to explore its potential as a novel therapeutic target in HNSCC.

We explored the significance of CLIC in HNSCC using cell biological analyses and investigated the gene expression profile of the CLIC2 forced-expressed HNSCC cell line. CLIC2 expression in human HNSCC was examined histopathologically.

Forced expression of CLIC2 in HNSCC cells was accompanied by increased cell proliferation, resistance against natural killer cells, and expression of tumor-promoting genes in addition to increased tumorigenicity upon xenografting in a mouse model. CLIC2 expression was observed in several human cases of HNSCC.

CLIC2 may act potentially as a novel risk factor for HNSCC.

论文信息

作者
Hosokawa Y、Miyoshi S、Hayashi Y、Irifune Y、Sato E、Mitani S、Choudhury M、Yano H
单位
Department of Otorhinolaryngology, Head and Neck Surgery, Graduate School of Medicine, Ehime University, Matsuyama, Ehime, Japan.Japan
文献类型
非美国政府资助研究
期刊
Head & neck2026 May
原文标识
PubMed 41386691 · DOI 10.1002/hed.70133