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BIOMARKER:
SERPINE1 expression
i
Other names: SERPINE1, Serpin Family E Member 1, PAI, PLANH1, PAI1, Serine (Or Cysteine) Proteinase Inhibitor, Clade E (Nexin, Plasminogen Activator Inhibitor Type 1), Member 1, Endothelial Plasminogen Activator Inhibitor, Plasminogen Activator Inhibitor 1, Serpin E1, PAI-1, Serpin Peptidase Inhibitor, Clade E (Nexin, Plasminogen Activator Inhibitor Type 1), Member 1, Plasminogen Activator Inhibitor, Type I
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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.
The NRG signature and its deep learning model have significant clinical implications, highlighting the importance of individualized treatment strategies based on GC subtyping. These findings provide valuable insights for guiding clinical decision-making and treatment approaches for GC.
1 year ago
Journal • IO biomarker
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SERPINE1 (Serpin Family E Member 1) • GPX3 (Glutathione Peroxidase 3)
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.
over 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.
over 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)
This study identified vital genes, pathways, and prognostic markers involved in the malignant transformation from normal oral tissue to OPL and primary OSCC, providing insights for early diagnosis and targeted therapy development. Cross-validation with an independent RNA-seq dataset and immunohistochemistry reinforced the findings, supporting the robustness of the identified molecular signatures.
over 1 year ago
Journal
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NFIB (Nuclear Factor I B) • SERPINE1 (Serpin Family E Member 1) • ITGA6 (Integrin, alpha 6)
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.
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.
This study found that miR-145-5p inhibits tumor progression and is expressed in lower amounts in patients with GC. MiR-145-5p was found to affect GC cell proliferation, migration, and invasion by negatively regulating SERPINE1 levels and controlling the ERK1/2 pathway.
over 1 year ago
Journal
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SERPINE1 (Serpin Family E Member 1) • MIR145 (MicroRNA 145)
In H1993-derived resistant cells, MEK inhibitors could be a potential therapeutic strategy for overcoming resistance with downstream mitogen-activated protein kinase pathway activation. In this study, we revealed the different mechanisms of acquired resistance to the MET inhibitor crizotinib with potential therapeutic application in patients with MET-amplified lung carcinoma.
over 1 year ago
Preclinical • Journal
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SERPINE1 (Serpin Family E Member 1)
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MET amplification • SERPINE1 expression • SERPINE1 overexpression
We provide the in vivo evidence of the clinical prognostic implications of therapy-induced senescence. Our results revealed that STCs were responsible for CRC progression by producing large amounts of EVs enriched in SERPINE1. These findings further confirm the crucial role of therapy-induced senescence in tumor progression and offer a potential therapeutic strategy for CRC treatment.
almost 2 years ago
Journal • Tumor cell
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SERPINE1 (Serpin Family E Member 1) • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
Through transcriptional profiling, we found that Serpine1 mRNA expression downregulates through TRA2B the expression of genes involved in the immune response. Analysis of human colon tumor samples showed an inverse correlation between SERPINE1 mRNA expression and CD8+ T cell infiltration, unveiling the potential value of SERPINE1 mRNA as a promising therapeutic target for colon tumors.
almost 2 years ago
Journal
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CD8 (cluster of differentiation 8) • SERPINE1 (Serpin Family E Member 1)