CLIC4 在人结直肠癌细胞中对岩藻黄质抑制生长敏感性的需求。
Requirement of CLIC4 Expression in Human Colorectal Cancer Cells for Sensitivity to Growth Inhibition by Fucoxanthinol.
机构信息
School of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Hokkaido, Japan.
Advanced Research Promotion Center, Health Sciences University of Hokkaido, Hokkaido, Japan.
出版信息
Cancer Genomics Proteomics. 2022 Jul-Aug;19(4):428-444. doi: 10.21873/cgp.20330.
BACKGROUND/AIM: Fucoxanthinol (FxOH), a marine carotenoid, induces apoptosis and anoikis in human colorectal cancer (CRC) DLD-1 cells via the down-regulation of chloride intracellular channel 4 (CLIC4) expression, a key molecule for apoptosis. However, whether FxOH is susceptible to CLIC4 expression and its regulatory mechanisms in human CRC cells remains unknown. We investigated the inhibitory effects of FxOH on six types of human CRC cells with CLIC4 regulation.
MATERIALS AND METHODS
The association between FxOH and CLIC4 was investigated using gene knockdown, overexpression, and transcriptome analyses.
RESULTS
CLIC4 expression in CRC cells was a significant factor associated with sensitivity to FxOH. CLIC4 regulates many cancer-related signals and participates in growth inhibition in FxOH-treated DLD-1 cells. Both CLIC4 knockdown and overexpression attenuated the inhibitory effects of FxOH on DLD-1 cells.
CONCLUSION
Our findings suggest that the protein expression of CLIC4 and its regulating mechanisms play significant roles regarding cell death in human CRC cells by FxOH treatment. Further investigation by in vitro and in vivo models is needed to determine the effect of CLIC4.
背景/目的：海洋类胡萝卜素岩藻黄质（FxOH）通过下调关键凋亡分子氯离子通道 4（CLIC4）的表达诱导人结直肠癌细胞（CRC）DLD-1 细胞凋亡和失巢凋亡。然而，FxOH 是否易受 CLIC4 表达及其在人 CRC 细胞中的调控机制的影响尚不清楚。我们研究了 FxOH 对 6 种具有 CLIC4 调控的人 CRC 细胞的抑制作用。
材料和方法
使用基因敲低、过表达和转录组分析研究了 FxOH 与 CLIC4 之间的关联。
结果
CRC 细胞中 CLIC4 的表达是与 FxOH 敏感性相关的重要因素。CLIC4 调节许多与癌症相关的信号，并参与 FxOH 处理的 DLD-1 细胞的生长抑制。CLIC4 的敲低和过表达均减弱了 FxOH 对 DLD-1 细胞的抑制作用。
结论
我们的研究结果表明，CLIC4 的蛋白表达及其调控机制在 FxOH 处理的人 CRC 细胞的细胞死亡中起着重要作用。需要通过体外和体内模型进一步研究 CLIC4 的作用。
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