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PTGER3 敲低抑制三阴性乳腺癌对铁死亡的脆弱性。

PTGER3 knockdown inhibits the vulnerability of triple-negative breast cancer to ferroptosis.

机构信息

Department of Pathology, Tianjin Medical University, Tianjin, China.

Department of Pathology, Tianjin Medical University General Hospital, Tianjin, China.

出版信息

Cancer Sci. 2024 Jun;115(6):2067-2081. doi: 10.1111/cas.16169. Epub 2024 Apr 2.

DOI:10.1111/cas.16169
PMID:38566528
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11145128/
Abstract

Prostaglandin E receptor 3 (PTGER3) is involved in a variety of biological processes in the human body and is closely associated with the development and progression of a variety of cancer types. However, the role of PTGER3 in triple-negative breast cancer (TNBC) remains unclear. In the present study, low PTGER3 expression was found to be associated with poor prognosis in TNBC patients. PTGER3 plays a crucial role in regulating TNBC cell invasion, migration, and proliferation. Upregulation of PTGER3 weakens the epithelial-mesenchymal phenotype in TNBC and promotes ferroptosis both in vitro and in vivo by repressing glutathione peroxidase 4 (GPX4) expression. On the other hand, downregulation of PTGER3 inhibits ferroptosis by increasing GPX4 expression and activating the PI3K-AKT pathway. Upregulation of PTGER3 also enhances the sensitivity of TNBC cells to paclitaxel. Overall, this study has elucidated critical pathways in which low PTGER3 expression protects TNBC cells from undergoing ferroptosis, thereby promoting its progression. PTGER3 may thus serve as a novel and promising biomarker and therapeutic target for TNBC.

摘要

前列腺素 E 受体 3（PTGER3）参与人体的多种生物学过程，与多种癌症类型的发生和发展密切相关。然而，PTGER3 在三阴性乳腺癌（TNBC）中的作用尚不清楚。本研究发现，PTGER3 低表达与 TNBC 患者的不良预后相关。PTGER3 在调节 TNBC 细胞侵袭、迁移和增殖方面起着关键作用。上调 PTGER3 通过抑制谷胱甘肽过氧化物酶 4（GPX4）的表达，在体外和体内减弱 TNBC 的上皮-间充质表型，并促进铁死亡。另一方面，下调 PTGER3 通过增加 GPX4 的表达和激活 PI3K-AKT 通路来抑制铁死亡。上调 PTGER3 还增强了 TNBC 细胞对紫杉醇的敏感性。总的来说，本研究阐明了低表达的 PTGER3 保护 TNBC 细胞免于发生铁死亡从而促进其进展的关键途径。因此，PTGER3 可能成为 TNBC 的一种新型有前途的生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2e6/11145128/975d9d874296/CAS-115-2067-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2e6/11145128/8f518365580f/CAS-115-2067-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2e6/11145128/801a97beb264/CAS-115-2067-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2e6/11145128/f9a39f4e9aae/CAS-115-2067-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2e6/11145128/060b0af3c040/CAS-115-2067-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2e6/11145128/36fec072ec97/CAS-115-2067-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2e6/11145128/7e4c31ed01c9/CAS-115-2067-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2e6/11145128/8f518365580f/CAS-115-2067-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2e6/11145128/801a97beb264/CAS-115-2067-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2e6/11145128/975d9d874296/CAS-115-2067-g001.jpg

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