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Ciz1 促进前列腺癌细胞的致瘤性。

Ciz1 promotes tumorigenicity of prostate carcinoma cells.

机构信息

Department of Urology, the First Hospital of China Medical University, Shenyang 110001, P. R. China.

出版信息

Front Biosci (Landmark Ed). 2015 Jan 1;20(4):705-15. doi: 10.2741/4331.

DOI:10.2741/4331
PMID:25553473
Abstract

Prostate cancer is the most common malignancy in men and is the second leading cause of cancer-related mortality in developed countries. Recent work has revealed the significance of CIP-interacting zinc finger protein 1 (CIZ1) in cancer cell biology, but its roles in prostatic carcinoma are unknown. Our study compared CIZ1 gene expression in banked prostatic carcinomas versus matched paraneoplastic tissues and in tumor cell lines of varying origin. This study revealed that the expression of CIZ1 was higher in high-grade prostate cancer than in low-grade prostate cancer and normal tissues. Among the tumor cell lines, PC-3 exhibited the highest levels of CIZ1 expression. CIZ1 gene silencing in PC-3 cells reduced cell proliferation and colony formation, induced cell cycle arrest in G1, inhibited tumor formation in nude mice, and suppressed the expression of genes related to prostate carcinoma. These results suggest that CIZ1 may play an important role in the progression of human prostate carcinoma and us which may be used as a therapeutic target in prostate cancer.

摘要

前列腺癌是男性最常见的恶性肿瘤,也是发达国家癌症相关死亡的第二大主要原因。最近的研究揭示了 CIP 相互作用锌指蛋白 1(CIZ1)在癌细胞生物学中的重要性,但它在前列腺癌中的作用尚不清楚。我们的研究比较了银行前列腺癌与配对副肿瘤组织以及不同来源的肿瘤细胞系中 CIZ1 基因的表达。这项研究表明,CIZ1 的表达在高级别前列腺癌中高于低级别前列腺癌和正常组织。在肿瘤细胞系中,PC-3 表现出最高水平的 CIZ1 表达。PC-3 细胞中 CIZ1 基因沉默降低了细胞增殖和集落形成,诱导 G1 期细胞周期停滞,抑制裸鼠肿瘤形成,并抑制与前列腺癌相关的基因表达。这些结果表明,CIZ1 可能在人类前列腺癌的进展中发挥重要作用,我们可以将其用作前列腺癌的治疗靶点。

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Ciz1 promotes tumorigenicity of prostate carcinoma cells.Ciz1 促进前列腺癌细胞的致瘤性。
Front Biosci (Landmark Ed). 2015 Jan 1;20(4):705-15. doi: 10.2741/4331.
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Epigenetic instability caused by absence of CIZ1 drives transformation during quiescence cycles.由于 CIZ1 的缺失导致的表观遗传不稳定性在静止周期中驱动转化。
BMC Biol. 2023 Aug 15;21(1):175. doi: 10.1186/s12915-023-01671-6.
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Prion-like domains drive CIZ1 assembly formation at the inactive X chromosome.
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J Cell Biol. 2022 Apr 4;221(4). doi: 10.1083/jcb.202103185. Epub 2022 Mar 15.
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Akt1 and dCIZ1 promote cell survival from apoptotic caspase activation during regeneration and oncogenic overgrowth.Akt1 和 dCIZ1 促进了再生和致癌过度生长过程中凋亡半胱天冬酶激活时的细胞存活。
Nat Commun. 2020 Nov 12;11(1):5726. doi: 10.1038/s41467-020-19068-2.
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