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BIOMARKER:
PAI1 expression
i
Other names: PAI1, Plasminogen Activator Inhibitor 1, Serpin E1, PLANH1, PAI-1, PAI, Serpin Peptidase Inhibitor, Clade E (Nexin, Plasminogen Activator Inhibitor Type 1), Member 1, Plasminogen Activator Inhibitor, Type I, Serpin Family E Member 1, Serine (Or Cysteine) Proteinase Inhibitor, Clade E (Nexin, Plasminogen Activator Inhibitor Type 1), Member 1, Endothelial Plasminogen Activator Inhibitor
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Chronic inflammation might explain part of the increased risk of CAD due to more or less severe excess weight, in a robust statistical mediation model.
Elevated expression of SERPINE1 in HNSCC is intricately linked with adverse prognostic outcomes and has the potential to influence the immune microenvironment. Subsequent investigations are imperative to fully elucidate the prognostic implications of SERPINE1 as a biomarker and to unlock its therapeutic promise as a target for intervention.
Activation of GPER1 reduces clonogenicity and migration of CSCC cells and suppresses expression of SERPINE1/PAI-1. Suppression of SERPINE1/PAI-1 in CSCC cells reduces tumorigenic potential. GPER1 may be a suitable target for suppression of SERPINE1/PAI-1 in CSCC. However, SERPINE1/PAI-1 does not appear to be the decisive factor for GPER1-regulated cell migration.
11 months ago
Preclinical • Journal
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SERPINE1 (Serpin Family E Member 1) • GPER1 (G Protein-Coupled Estrogen Receptor 1)
This study reveals that MESB is crucial in preventing hepatic fibrosis via the cPLA2-mediated arachidonic acid metabolic pathway, highlighting its key active components as potential drugs for fibrosis treatment.
Importantly, miR-642a-3p knockdown suppressed growth and EMT in orthotopic liver tumors. CAF-derived miR-642a-3p/SERPINE1 axis facilitated migration, invasion, and EMT in the HCC cells, suggesting miR-642a-3p/SERPINE1 axis can be a potential therapeutic target for HCC.
Drug sensitivity to the HER2 kinase inhibitor lapatinib was characterized under conditions of monoculture and exposure to breast fibroblast-conditioned medium...Combination therapies targeting HER2 kinase and these fibroblast-induced signaling adaptations eliminates fibroblast-protected HER2+ breast cancer cells. The online version contains supplementary material available at 10.1007/s12195-024-00823-0.
Based on the findings in this study, suppressing PAI1 expression in VC cells appears to reduce their progression and tumorigenic potential. Therefore, PAI1 could possibly function as an oncogene in VC. GPER1 appears to be a suitable target for suppressing PAI1 in VC.
1 year ago
Journal
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ER (Estrogen receptor) • SERPINE1 (Serpin Family E Member 1) • GPER1 (G Protein-Coupled Estrogen Receptor 1)
LINC00665 sponged miR-199b-5p to interact with SERPINE1 expression, resulting in the increase of phosphorylation of AKt, thus participating in the PI3K/AKt pathway. To summarize, LINC00665 facilitated the tumorigenesis and trastuzumab resistance of GC by sponging miR-199b-5p and promoting SERPINE1 expression, which further activated PI3K/AKt signaling; this finding reveals a new mechanism by which LINC00665 modulates tumor development and drug resistance in GC.
1 year ago
Journal
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MIR199B (MicroRNA 199b) • SERPINE1 (Serpin Family E Member 1) • LINC00665 (Long Intergenic Non-Protein Coding RNA 665)
Collectively, our findings revealed that GDNF upregulated SERPINE1 via the SMAD2/3-signaling pathway, thereby accelerating GBM cell migration and invasion. The present work presents a new mechanism of GDNF, supporting GBM development.
Taken together, these data support a role for platelet PI3Kβ in promoting breast cancer metastasis and highlight platelet PI3Kβ as a potential therapeutic target. We demonstrate that platelet PI3Kβ regulates metastasis, broadening the potential use of PI3Kβ-selective inhibitors as novel agents to treat metastasis.
Treatment of MCF-7 cells with paclitaxel (PTX), a microtubule-stabilizing antitumor drug, at 1 µM for 2 h elevated the PAI-1 concentration of the conditioned medium at 48 h after treatment but not in those treated with tamoxifen and cyclophosphamide. Microtubule assembly inhibitors vinblastine (VBT) and vincristine (VCT) also increased the PAI-1 concentration in the conditioned medium...This study demonstrated that temporary low-dose treatment with microtubule-associated anticancer drugs increased PAI-1 release from MCF-7 cells but not from MDA-MB-231 cells. These results indicate that chemotherapy against luminal A-type breast cancer using microtubule-associated drugs may cause thrombosis through the inhibition of the fibrinolytic system by PAI-1.
Moreover, in breast cancer tissues, we found that the expression of PAIP1 was positively correlated with cyclin E2. Taken together, our findings establish the role and mechanism of PAIP1 in breast cancer progression, indicating that PAIP1 would be a new therapeutic target for breast cancer treatment.