Division of Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Division of Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan
Anticancer Res. 2022 Jan;42(1):271-277. doi: 10.21873/anticanres.15482.
BACKGROUND/AIM: Chloride intracellular channel 1 (CLIC1) is a member of the chloride channel protein family. The aim of this study was to clarify the role of CLIC1 in lung adenocarcinoma.
The expression levels of CLIC1 in 74 patients with completely resected lung adenocarcinoma were analyzed by immunohistochemistry. Overall survival was assessed in relation to the expression level of CLIC1. Moreover, in the lung cancer cell lines A549 and PC9, CLIC1 expression was inhibited by small interfering RNA. The function of CLIC1 was analyzed in these cell lines.
High expression of CLIC1 was associated with short overall survival compared to low expression (p=0.0327). Multivariate analysis revealed that CLIC1 expression was an independent prognostic factor. Knockdown of CLIC1 inhibited cell proliferation and migration through suppression of the p38 MAPK signaling pathway in A549 and PC9 cells.
CLIC1 may be a useful prognostic factor in lung adenocarcinoma.
背景/目的：氯离子细胞内通道 1（CLIC1）是氯离子通道蛋白家族的一员。本研究旨在阐明 CLIC1 在肺腺癌中的作用。
通过免疫组织化学分析了 74 例完全切除的肺腺癌患者中 CLIC1 的表达水平。根据 CLIC1 的表达水平评估总生存率。此外，在肺癌细胞系 A549 和 PC9 中，通过小干扰 RNA 抑制 CLIC1 的表达。在这些细胞系中分析了 CLIC1 的功能。
与低表达相比，CLIC1 的高表达与总生存期短相关（p=0.0327）。多变量分析显示，CLIC1 表达是独立的预后因素。CLIC1 的敲低通过抑制 A549 和 PC9 细胞中的 p38 MAPK 信号通路抑制细胞增殖和迁移。
CLIC1 可能是肺腺癌中有用的预后因素。
