NOL6 Promotes Tumor Progression by Facilitating Cancer Cell-Induced Platelet Aggregation and Angiogenesis in Breast Cancer.

IF 3.3 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Tingting Zhang, Cheng Lu, Mingming Lv, Shengwang Du, Xinjun Wu
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引用次数: 0

Abstract

Background: Breast cancer (BC) is a prevalent malignancy among women, and numerous investigations have reported that platelet aggregation may play a role in BC progression. Thus, identifying new targets for BC is essential. In this regard, we focused on nucleolar protein 6 (NOL6), located on chromosome 9p13, which is implicated in tumor development.

Objective: To investigate NOL6 expression in BC, examine its role in platelet aggregation and angiogenesis, and elucidate the underlying mechanisms.

Methods: Bioinformatic analyses, immunoblotting, and quantitative real-time polymerase chain reaction (qPCR) were performed to assess NOL6 expression in BC. Cell counting kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assays were conducted to determine the impact of NOL6 on BC cell proliferation. Immunostaining, enzyme-linked immunosorbent assay (ELISA), and flow cytometry (FCM) assays were utilized to analyze the effects of NOL6 on platelet aggregation. Tube formation and transwell assays were performed to examine angiogenesis and invasion, immunoblot assays were used to confirm the underlying mechanisms, and tumor growth assays in mice were conducted to validate the findings in vivo.

Results: NOL6 was found to be highly expressed in BC and was associated with patient prognosis, platelet aggregation, and angiogenesis. Its knockdown inhibited BC cell proliferation and reduced platelet aggregation induced by BC cells. Additionally, NOL6 depletion impaired angiogenesis and migration of BC cells. In vivo studies confirmed that NOL6 promotes tumor growth. Mechanistically, NOL6 enhances the Twisted spiral transcription factor 1 (Twist1)/galectin-3 axis, contributing to BC progression.

Conclusions: NOL6 can promote tumor progression by facilitating platelet aggregation and angiogenesis in BC cells through the Twist1/galectin-3 axis.

在乳腺癌中,NOL6通过促进癌细胞诱导的血小板聚集和血管生成促进肿瘤进展。
背景:乳腺癌(BC)是女性中常见的恶性肿瘤,许多研究报道血小板聚集可能在BC的进展中起作用。因此,确定BC的新靶点至关重要。在这方面,我们重点研究了位于染色体9p13上的核仁蛋白6 (NOL6),它与肿瘤的发展有关。目的:研究NOL6在BC中的表达,探讨其在血小板聚集和血管生成中的作用,并探讨其机制。方法:采用生物信息学分析、免疫印迹和定量实时聚合酶链反应(qPCR)方法检测NOL6在BC中的表达。通过细胞计数试剂盒-8 (CCK-8)和5-乙基-2′-脱氧尿苷(EdU)测定测定NOL6对BC细胞增殖的影响。采用免疫染色、酶联免疫吸附法(ELISA)和流式细胞术(FCM)分析NOL6对血小板聚集的影响。通过试管形成和transwell实验来检测血管生成和侵袭,免疫印迹实验来确认潜在的机制,在小鼠体内进行肿瘤生长实验来验证这些发现。结果:在BC中发现NOL6高表达,并与患者预后、血小板聚集和血管生成相关。它的敲除抑制了BC细胞的增殖,降低了BC细胞诱导的血小板聚集。此外,NOL6缺失会损害BC细胞的血管生成和迁移。体内研究证实,NOL6促进肿瘤生长。在机制上,NOL6增强了扭曲螺旋转录因子1 (Twist1)/半乳糖凝集素-3轴,促进了BC的进展。结论:NOL6通过Twist1/galectin-3轴促进BC细胞血小板聚集和血管生成,从而促进肿瘤进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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