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三阴性乳腺癌细胞中 IRAK2 的下调可降低细胞体外生长,并延缓小鼠模型中的肿瘤进展。

IRAK2 Downregulation in Triple-Negative Breast Cancer Cells Decreases Cellular Growth In Vitro and Delays Tumour Progression in Murine Models.

机构信息

Department of Obstetrics and Gynecology, University Hospital Aachen (UKA), D-52074 Aachen, Germany.

Pathology Institute, University Hospital Aachen (UKA), D-52074 Aachen, Germany.

出版信息

Int J Mol Sci. 2023 Jan 28;24(3):2520. doi: 10.3390/ijms24032520.

DOI:10.3390/ijms24032520
PMID:36768848
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9917074/
Abstract

Breast cancer stem cells (BCSCs) are responsible for tumour recurrence and therapy resistance. We have established primary BCSC cultures from human tumours of triple-negative breast cancer (TNBC), a subgroup of breast cancer likely driven by BCSCs. Primary BCSCs produce xenografts that phenocopy the tumours of origin, making them an ideal model for studying breast cancer treatment options. In the TNBC cell line MDA-MB-468, we previously screened kinases whose depletion elicited a differentiation response, among which IRAK2 was identified. Because primary BCSCs are enriched in IRAK2, we wondered whether IRAK2 downregulation might affect cellular growth. IRAK2 was downregulated in primary BCSCs and MDA-MB-468 by lentiviral delivery of shRNA, causing a decrease in cellular proliferation and sphere-forming capacity. When orthotopically transplanted into immunocompromised mice, IRAK2 knockdown cells produced smaller xenografts than control cells. At the molecular level, IRAK2 downregulation reduced NF-κB and ERK phosphorylation, IL-6 and cyclin D1 expression, ERN1 signalling and autophagy in a cell line-dependent way. Overall, IRAK2 downregulation decreased cellular aggressive growth and pathways often exploited by cancer cells to endure stress; therefore, IRAK2 may be considered an interesting target to compromise TNBC progression.

摘要

乳腺癌干细胞(BCSCs)是肿瘤复发和治疗耐药的原因。我们已经从三阴性乳腺癌(TNBC)的人类肿瘤中建立了原发性 BCSC 培养物,这是一种可能由 BCSC 驱动的乳腺癌亚组。原发性 BCSC 产生的异种移植物可模拟起源肿瘤的表型,使其成为研究乳腺癌治疗选择的理想模型。在 TNBC 细胞系 MDA-MB-468 中,我们之前筛选了那些缺失会引起分化反应的激酶,其中 IRAK2 被鉴定出来。由于原发性 BCSC 中 IRAK2 富集,我们想知道 IRAK2 下调是否会影响细胞生长。通过慢病毒递送 shRNA 下调原发性 BCSC 和 MDA-MB-468 中的 IRAK2,导致细胞增殖和球体形成能力下降。当将 IRAK2 敲低细胞原位移植到免疫缺陷小鼠中时,与对照细胞相比,IRA K2 敲低细胞产生的异种移植物更小。在分子水平上,IRAK2 下调以依赖细胞系的方式降低 NF-κB 和 ERK 磷酸化、IL-6 和细胞周期蛋白 D1 表达、ERN1 信号和自噬。总的来说,IRAK2 下调降低了细胞侵袭性生长和癌细胞经常用来耐受应激的途径;因此,IRAK2 可能被认为是一个有前途的靶点,可以削弱 TNBC 的进展。

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