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细菌脂多糖诱导的蓬乱蛋白片段极性蛋白 3(DVL3)通过 TLR4 通路促进前列腺癌细胞的增殖和迁移。

Dishevelled Segment Polarity Protein 3 (DVL3) Induced by Bacterial LPS Promotes the Proliferation and Migration of Prostate Cancer Cells through the TLR4 Pathway.

机构信息

Department of Oncology, Qingdao Municipal Hospital, Shandong University, 266012 Qingdao, Shandong, China.

Pulmonary and Critical Care Medicine, Rongcheng City People's Hospital, 264300 Weihai, Shandong, China.

出版信息

Arch Esp Urol. 2024 Mar;77(2):193-201. doi: 10.56434/j.arch.esp.urol.20247702.25.

DOI:10.56434/j.arch.esp.urol.20247702.25
PMID:38583012
Abstract

BACKGROUND

Chronic inflammation is associated with various malignant tumors. Bacterial lipopolysaccharides (LPSs) play a significant part in the event and development of prostate cancer. Dishevelled segment polarity protein 3 () is a shared component of the Wnt/β-catenin and Notch signaling pathways, which are involved in tumor progression, chemoresistance, and maintenance of stem cell-like properties. According to reports, prostatic cancer cell invasion and proliferation are mediated by toll-like receptor 4 (). However, the role and regulation of in prostate cancer and its relationship with remain unclear.

METHODS

Survival curves were plotted to evaluate the relationship between expression and prognosis in patients with prostate cancer. was silenced in PC3 and DU145 cells using small interfering RNAs (siRNAs). Subsequently, cell counting kit-8 (CCK-8) assay, colony formation assay, transwell migration assay, and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) were performed to investigate the role of in cell proliferation and migration . The protein markers of potential pathways were analyzed via western blotting.

RESULTS

expression was linked to prognosis in patients with prostate cancer; In particular, patients with high expression had a poor prognosis. LPS stimulation increased ( < 0.01) the expression of in PC3 cells. regulated tumor cell proliferation and migration by mediating the increase ( < 0.01) in expression. Knockout of validated that played a crucial role in LPS-induced expression. Silencing of decreased ( < 0.01) the LPS-induced proliferation and migration of PC3 cells.

CONCLUSIONS

Bacterial LPS-induced promoted the multiplication and migration of prostate cancer cells through the pathway. This study offers a valuable reference for the development and clinical application of targeted drugs for prostate cancer.

摘要

背景

慢性炎症与各种恶性肿瘤有关。细菌脂多糖(LPS)在前列腺癌的发生和发展中起重要作用。蓬乱蛋白片段极性蛋白 3()是 Wnt/β-连环蛋白和 Notch 信号通路的共有成分,参与肿瘤进展、化疗耐药和维持干细胞样特性。据报道,前列腺癌细胞的侵袭和增殖是由 Toll 样受体 4()介导的。然而,在前列腺癌中及其与的关系尚不清楚。

方法

通过绘制生存曲线来评估 表达与前列腺癌患者预后的关系。使用小干扰 RNA(siRNA)沉默 PC3 和 DU145 细胞中的。随后,通过细胞计数试剂盒-8(CCK-8)检测、集落形成实验、Transwell 迁移实验和实时定量聚合酶链反应(qRT-PCR)检测在细胞增殖和迁移中的作用。通过 Western blot 分析潜在途径的蛋白标志物。

结果

表达与前列腺癌患者的预后相关;特别是高表达的患者预后不良。LPS 刺激增加(<0.01)PC3 细胞中表达。通过介导表达的增加(<0.01),调节肿瘤细胞的增殖和迁移。敲除验证了在 LPS 诱导的表达中起关键作用。沉默降低了 LPS 诱导的 PC3 细胞的增殖和迁移(<0.01)。

结论

细菌 LPS 诱导的促进了前列腺癌细胞的增殖和迁移,通过途径。本研究为前列腺癌靶向药物的开发和临床应用提供了有价值的参考。

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