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CCDC154基因敲低通过抑制Snail的表达来抑制肝癌生长。

CCDC154 knockdown inhibits growth of liver cancer via suppressing expression of Snail.

作者信息

Ma Rulan, Nie Hongmei, Mo Caijing, Yuan Dawei, Zhu Kun, Li Kang

机构信息

Department of Surgical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, 277 West Yanta Road, Xi'an, 710061, Shaanxi, China.

Department of Obstetrics and Gynecology, The Public Hospital of Feicheng, Feicheng, 271600, Shandong, China.

出版信息

Eur J Med Res. 2025 Jan 30;30(1):59. doi: 10.1186/s40001-025-02290-3.

DOI:10.1186/s40001-025-02290-3
PMID:39885494
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11781066/
Abstract

OBJECTIVE

The effect of coiled-coil domain-containing 154 (CCDC154) in liver cancer (LC) remains unexplored. The objective of this study was to investigate the role of CCDC154 in LC and its underlying mechanism.

METHODS

The analysis of CCDC154 expression and prognosis was performed using UALCAN, Human Protein Atlas and Kaplan-Meier plotter websites. Protein expression was measured using Western blotting assay. Lentivirus was used to silence CCDC154 expression in LC cells. The proliferation and apoptosis of LC cells was evaluated by cell counting assay, colony formation assay and flow cytometry. The migration and invasion of LC cells were investigated using scratch wound-healing assay and Transwell assay.

RESULTS

The results showed that CCDC154 was highly expressed in LC and related to tumor grade and stage. High CCDC154 expression was associated with to poor outcomes in LC patients. Silencing of CCDC154 inhibited proliferation, migration and invasion of LC cells. It also increased apoptosis in LC cells. After CCDC154 knockdown, the expression of Twist, Vimentin and Snail was down-regulated. Overexpression of Snail abated the inhibitory caused by CCDC154 knockdown on LC cell growth.

CONCLUSION

CCDC154 knockdown suppressed LC development through reducing Snail expression.

摘要

目的

含卷曲螺旋结构域蛋白154(CCDC154)在肝癌(LC)中的作用尚未明确。本研究旨在探讨CCDC154在肝癌中的作用及其潜在机制。

方法

利用UALCAN、人类蛋白质图谱和Kaplan-Meier绘图仪网站对CCDC154表达及预后进行分析。采用蛋白质印迹法检测蛋白表达。利用慢病毒沉默肝癌细胞中CCDC154的表达。通过细胞计数法、集落形成试验和流式细胞术评估肝癌细胞的增殖和凋亡。采用划痕愈合试验和Transwell试验研究肝癌细胞的迁移和侵袭能力。

结果

结果显示,CCDC154在肝癌中高表达,且与肿瘤分级和分期相关。CCDC154高表达与肝癌患者不良预后相关。沉默CCDC154可抑制肝癌细胞的增殖、迁移和侵袭。它还增加了肝癌细胞的凋亡。敲低CCDC154后,Twist、波形蛋白和Snail的表达下调。过表达Snail可减轻CCDC154敲低对肝癌细胞生长的抑制作用。

结论

敲低CCDC154通过降低Snail表达抑制肝癌发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40be/11781066/ec03735f9037/40001_2025_2290_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40be/11781066/1ff4623afbc6/40001_2025_2290_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40be/11781066/ef50686ad2e3/40001_2025_2290_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40be/11781066/c66086145fb8/40001_2025_2290_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40be/11781066/0a5f1e975bd4/40001_2025_2290_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40be/11781066/ec03735f9037/40001_2025_2290_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40be/11781066/1ff4623afbc6/40001_2025_2290_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40be/11781066/ef50686ad2e3/40001_2025_2290_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40be/11781066/c66086145fb8/40001_2025_2290_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40be/11781066/0a5f1e975bd4/40001_2025_2290_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40be/11781066/ec03735f9037/40001_2025_2290_Fig5_HTML.jpg

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本文引用的文献

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CBX1 is involved in hepatocellular carcinoma progression and resistance to sorafenib and lenvatinib via IGF-1R/AKT/SNAIL signaling pathway.CBX1 通过 IGF-1R/AKT/SNAIL 信号通路参与肝细胞癌的进展和对索拉非尼及仑伐替尼的耐药性。
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Plumbagin Regulates Snail to Inhibit Hepatocellular Carcinoma Epithelial-Mesenchymal Transition in vivo and in vitro.
白花丹素通过调控蜗牛蛋白抑制肝癌细胞上皮-间质转化的体内外研究
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DNA methylation-mediated high expression of CCDC50 correlates with poor prognosis and hepatocellular carcinoma progression.CCDC50 的高表达与 DNA 甲基化相关,与预后不良和肝癌进展相关。
Aging (Albany NY). 2023 Aug 7;15(15):7424-7439. doi: 10.18632/aging.204899.
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