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首页> 外文期刊>Journal of Investigative Dermatology Symposium Proceedings >CLIC4, an Intracellular Chloride Channel Protein, Is a Novel Molecular Target for Cancer Therapy
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CLIC4, an Intracellular Chloride Channel Protein, Is a Novel Molecular Target for Cancer Therapy

机译：CLIC4，一种细胞内氯离子通道蛋白，是癌症治疗的一种新型分子靶标。

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摘要

Chloride intracellular channel (CLIC)4 is a p53- and tumor necrosis factor (TNF)-regulated chloride channel protein that is localized to the mitochondria and cytoplasm of mouse and human keratinocytes. CLIC4 protein increases in differentiating keratinocytes and in keratinocytes exposed to DNA-damaging agents and metabolic inhibitors. Increasing CLIC4 levels by transduction of recombinant CLIC4 causes apoptosis. CLIC4 translocates to the nucleus under a variety of conditions of cell stress, and nuclear CLIC4 is associated with cell cycle arrest and accelerated apoptosis. Reduction of CLIC4 and several other CLIC family members by expressing a doxycycline-regulated CLIC4 antisense also causes apoptosis in squamous cancer cell lines. Expressing antisense CLIC4 in tumors derived from transplanting these cells into nude mice inhibits tumor growth, increases tumor apoptosis, and reduces tumor cell proliferation. Co-administration of TNF intraperitoneally enhances the tumor-inhibitory influence of CLIC4 antisense expression. Together, these results suggest that CLIC4 is important for keratinocyte viability and may be a novel target for anti-cancer therapy.
机译：氯离子细胞内通道（CLIC）4是p53和肿瘤坏死因子（TNF）调节的氯离子通道蛋白，位于小鼠和人角质形成细胞的线粒体和细胞质中。 CLIC4蛋白在分化的角质形成细胞以及暴露于DNA破坏剂和代谢抑制剂的角质形成细胞中增加。通过重组CLIC4的转导增加CLIC4水平会导致细胞凋亡。 CLIC4在多种细胞应激条件下易位至细胞核，而核CLIC4与细胞周期停滞和细胞凋亡加速相关。通过表达强力霉素调节的CLIC4反义物减少CLIC4和其他几个CLIC家族成员也导致鳞状癌细胞系凋亡。在将这些细胞移植到裸鼠后衍生的肿瘤中表达反义CLIC4抑制肿瘤生长，增加肿瘤细胞凋亡，并减少肿瘤细胞增殖。腹膜内共同施用TNF可增强CLIC4反义表达对肿瘤的抑制作用。在一起，这些结果表明CLIC4对角质形成细胞的生存能力很重要，并且可能是抗癌治疗的新目标。

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