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PTTG1通过cGMP-PKG信号通路促进M2巨噬细胞极化，并促进人上皮性卵巢癌细胞的上皮-间质转化进程。

PTTG1 promotes M2 macrophage polarization via the cGMP-PKG signaling pathway and facilitates EMT progression in human epithelial ovarian cancer cells.

作者信息

Tian Liang, Liu Liyun, Wang Chunlou, Kong Yan, Miao Zhigang, Yao Qing, Zhang He, Li Yuehong

机构信息

Department of Pathology, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Xinhua District, Shijiazhuang, 050000, China.

Department of Pathology, Cangzhou Central Hospital, Cangzhou, 061000, China.

出版信息

Discov Oncol. 2025 May 12;16(1):730. doi: 10.1007/s12672-025-02512-4.

DOI:10.1007/s12672-025-02512-4
PMID:40353994
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12069767/
Abstract

Epithelial Ovarian Cancer (EOC) is complex and heterogeneous, making accurate prognosis and treatment prediction difficult. New therapeutic targets and their mechanisms are urgently needed. This study explored the role of PTTG1 in ovarian cancer via the cGMP-PKG signaling pathway, focusing on its effects on M2 macrophage polarization and EMT progression in EOC cells. Using the GSE135886 database, we performed differential gene expression, pathway enrichment, and immune infiltration analyses to identify key targets influencing EMT and macrophage polarization. We then constructed PTTG1 knockdown and overexpression cell lines to assess the impact of PTTG1 on cell proliferation, migration, invasion, EMT, and macrophage polarization in vitro. Analysis revealed that differentially expressed genes were enriched in the cGMP-PKG pathway and correlated with M2 macrophages. PTTG1 overexpression in A2780 and SK-OV-3 ovarian cancer cells promoted proliferation, invasion, and migration, while enhancing sGC, PKG1, and PKG2 expression to activate the cGMP-PKG pathway and induce M2 macrophage polarization. PTTG1 knockdown produced opposite results, reinforcing our conclusions. This study uncovers a novel mechanism of PTTG1 in ovarian cancer development and suggests it as a potential therapeutic target.

摘要

上皮性卵巢癌（EOC）复杂且具有异质性，使得准确的预后和治疗预测变得困难。迫切需要新的治疗靶点及其作用机制。本研究通过cGMP-PKG信号通路探讨了PTTG1在卵巢癌中的作用，重点关注其对EOC细胞中M2巨噬细胞极化和上皮-间质转化（EMT）进程的影响。利用GSE135886数据库，我们进行了差异基因表达、通路富集和免疫浸润分析，以确定影响EMT和巨噬细胞极化的关键靶点。然后我们构建了PTTG1敲低和过表达细胞系，以评估PTTG1对体外细胞增殖、迁移、侵袭、EMT和巨噬细胞极化的影响。分析表明，差异表达基因在cGMP-PKG通路中富集，并与M2巨噬细胞相关。在A2780和SK-OV-3卵巢癌细胞中过表达PTTG1可促进增殖、侵袭和迁移，同时增强可溶性鸟苷酸环化酶（sGC）、蛋白激酶G1（PKG1）和蛋白激酶G2（PKG2）的表达，以激活cGMP-PKG通路并诱导M2巨噬细胞极化。PTTG1敲低产生相反的结果，强化了我们的结论。本研究揭示了PTTG1在卵巢癌发生发展中的一种新机制，并表明它是一个潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60e1/12069767/a103dd7eb7ac/12672_2025_2512_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60e1/12069767/61d28010a169/12672_2025_2512_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60e1/12069767/1bcdc6062b31/12672_2025_2512_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60e1/12069767/abb12afe2d5b/12672_2025_2512_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60e1/12069767/53dbc0ce462e/12672_2025_2512_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60e1/12069767/81f143cae2a3/12672_2025_2512_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60e1/12069767/a103dd7eb7ac/12672_2025_2512_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60e1/12069767/61d28010a169/12672_2025_2512_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60e1/12069767/1bcdc6062b31/12672_2025_2512_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60e1/12069767/abb12afe2d5b/12672_2025_2512_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60e1/12069767/53dbc0ce462e/12672_2025_2512_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60e1/12069767/81f143cae2a3/12672_2025_2512_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60e1/12069767/a103dd7eb7ac/12672_2025_2512_Fig6_HTML.jpg

相似文献

[1]
PTTG1 promotes M2 macrophage polarization via the cGMP-PKG signaling pathway and facilitates EMT progression in human epithelial ovarian cancer cells.

Discov Oncol. 2025-5-12

[2]
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Eur J Med Res. 2025-1-7

[3]
CTHRC1 in Ovarian Cancer Promotes M2-Like Polarization of Tumor-Associated Macrophages via Regulation of the STAT6 Signaling Pathway.

Onco Targets Ther. 2020-6-17

[4]
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Int Immunopharmacol. 2025-4-24

[5]
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Ann Transl Med. 2022-9

[6]
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J Inflamm Res. 2024-7-12

[7]
Lysine demethylase 2A promotes the progression of ovarian cancer by regulating the PI3K pathway and reversing epithelial‑mesenchymal transition.

Oncol Rep. 2018-11-27

[8]
8-Br-cGMP suppresses tumor progression through EGFR/PLC γ1 pathway in epithelial ovarian cancer.

Mol Biol Rep. 2024-1-18

[9]
VASP Knockdown Ameliorates Lipopolysaccharide-Induced Acute Lung Injury with Inhibition of M1 Macrophage Polarization Through the cGMP-PKG Signaling Pathway.

Inflammation. 2025-3-5

[10]
PTTG1 cooperated with GLI1 leads to epithelial-mesenchymal transition in esophageal squamous cell cancer.

Oncotarget. 2017-9-27

本文引用的文献

[1]
The Role of RAC2 and PTTG1 in Cancer Biology.

Cells. 2025-2-23

[2]
The Current State of the Diagnoses and Treatments for Clear Cell Renal Cell Carcinoma.

Cancers (Basel). 2024-12-1

[3]
Multi-omics analysis identifies PTTG1 as a prognostic biomarker associated with immunotherapy and chemotherapy resistance.

BMC Cancer. 2024-10-25

[4]
Inflammation-Related Gene ADH1A Regulates the Polarization of Macrophage M1 and Influences the Malignant Progression of Gastric Cancer.

J Inflamm Res. 2024-7-12

[5]
Prognostic Significance of CD163+ and/or CD206+ Tumor-Associated Macrophages Is Linked to Their Spatial Distribution and Tumor-Infiltrating Lymphocytes in Breast Cancer.

Cancers (Basel). 2024-6-5

[6]
Cancer Stage Compared With Mortality as End Points in Randomized Clinical Trials of Cancer Screening: A Systematic Review and Meta-Analysis.

JAMA. 2024-6-11

[7]
Global epidemiology of epithelial ovarian cancer.

Nat Rev Clin Oncol. 2024-5

[8]
PTTG1 induces pancreatic cancer cell proliferation and promotes aerobic glycolysis by regulating c-myc.

Open Life Sci. 2024-2-8

[9]
Protocols for Co-Culture Phenotypic Assays with Breast Cancer Cells and THP-1-Derived Macrophages.

J Mammary Gland Biol Neoplasia. 2024-2-10

[10]
8-Br-cGMP suppresses tumor progression through EGFR/PLC γ1 pathway in epithelial ovarian cancer.

Mol Biol Rep. 2024-1-18

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