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NOTCH3 通过直接调控 SPP1 和激活 PI3K/AKT 通路促进膀胱癌的恶性进展。

NOTCH3 promotes malignant progression of bladder cancer by directly regulating SPP1 and activating PI3K/AKT pathway.

机构信息

Department of Urology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.

Urinary Diseases Clinical Medical Research Center of Qingdao, Qingdao, Shandong, China.

出版信息

Cell Death Dis. 2024 Nov 18;15(11):840. doi: 10.1038/s41419-024-07241-0.

Abstract

The biological role and precise molecular mechanisms of Notch receptor 3 (NOTCH3) in the malignant progression of bladder cancer (BLCA) remain unclear. In this study, we found that NOTCH3 was significantly upregulated and associated with poor prognosis in BLCA patients. Functional experiments demonstrated that NOTCH3 knockdown inhibited BLCA cell proliferation, migration, invasion and significantly suppressed tumor growth and metastasis in vivo as well. Mechanically, chromatin immunoprecipitation and dual-luciferase reporter assays confirmed that NOTCH3 could promote the transcription of secreted phosphoprotein 1 (SPP1), a potential downstream target gene of NOTCH3, by binding to the CSL elements in the SPP1 promoter. Moreover, we also found that targeting NOTCH3 inhibited BLCA growth and metastasis by suppressing the SPP1-PI3K/AKT axis. Our study highlights the critical role of NOTCH3-SPP1-PI3K/AKT axis in the malignant progression of BLCA, suggesting that NOTCH3 may be a potential therapeutic target for BLCA.

摘要

Notch 受体 3(NOTCH3)在膀胱癌(BLCA)恶性进展中的生物学作用和精确分子机制尚不清楚。在本研究中,我们发现 NOTCH3 在 BLCA 患者中显著上调,并与预后不良相关。功能实验表明,NOTCH3 敲低抑制了 BLCA 细胞的增殖、迁移和侵袭,并显著抑制了体内肿瘤的生长和转移。机制上,染色质免疫沉淀和双荧光素酶报告基因检测证实,NOTCH3 通过与 SPP1 启动子中的 CSL 元件结合,可促进分泌型磷蛋白 1(SPP1)的转录,SPP1 是 NOTCH3 的一个潜在下游靶基因。此外,我们还发现,通过抑制 SPP1-PI3K/AKT 轴,靶向 NOTCH3 可抑制 BLCA 的生长和转移。我们的研究强调了 NOTCH3-SPP1-PI3K/AKT 轴在 BLCA 恶性进展中的关键作用,提示 NOTCH3 可能是 BLCA 的一个潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2114/11574029/3e912e3ead2f/41419_2024_7241_Fig1_HTML.jpg

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