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BIOMARKER:

SERPINE1 expression

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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
Entrez ID:
Related biomarkers:
1year
CAF-derived miR-642a-3p supports migration, invasion, and EMT of hepatocellular carcinoma cells by targeting SERPINE1. (PubMed, PeerJ)
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.
Journal
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SERPINE1 (Serpin Family E Member 1)
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PAI1 expression • SERPINE1 expression
1year
Integrating transcriptomic data and digital pathology for NRG-based prediction of prognosis and therapy response in gastric cancer. (PubMed, Ann Med)
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.
Journal • IO biomarker
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SERPINE1 (Serpin Family E Member 1) • GPX3 (Glutathione Peroxidase 3)
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SERPINE1 expression
over1year
Suppressing Expression of SERPINE1/PAI1 Through Activation of GPER1 Reduces Progression of Vulvar Carcinoma. (PubMed, Cancer Genomics Proteomics)
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.
Journal
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ER (Estrogen receptor) • SERPINE1 (Serpin Family E Member 1) • GPER1 (G Protein-Coupled Estrogen Receptor 1)
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PAI1 expression • SERPINE1 expression
over1year
Targeting LINC00665/miR-199b-5p/SERPINE1 axis to inhibit trastuzumab resistance and tumorigenesis of gastric cancer via PI3K/AKt pathway. (PubMed, Noncoding RNA Res)
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.
Journal
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MIR199B (MicroRNA 199b) • SERPINE1 (Serpin Family E Member 1) • LINC00665 (Long Intergenic Non-Protein Coding RNA 665)
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PAI1 expression • SERPINE1 expression
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Herceptin (trastuzumab)
over1year
Malignant Transformation of Normal Oral Tissue to Dysplasia and Early Oral Squamous Cell Carcinoma: An In Silico Transcriptomics Approach. (PubMed, Anal Cell Pathol (Amst))
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.
Journal
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NFIB (Nuclear Factor I B) • SERPINE1 (Serpin Family E Member 1) • ITGA6 (Integrin, alpha 6)
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SERPINE1 expression • SERPINE1 overexpression
over1year
Preclinical • Journal
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SERPINE1 (Serpin Family E Member 1)
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SERPINE1 expression • SERPINE1 overexpression
over1year
Glial-Cell-Line-Derived Neurotrophic Factor Promotes Glioblastoma Cell Migration and Invasion via the SMAD2/3-SERPINE1-Signaling Axis. (PubMed, Int J Mol Sci)
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.
Preclinical • Journal
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SERPINE1 (Serpin Family E Member 1)
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PAI1 expression • SERPINE1 expression
over1year
Paclitaxel and Vinblastine Increase Plasminogen Activator Inhibitor-1 Production in Human Breast Cancer MCF-7 Cells but Not MDA-MB-231 Cells. (PubMed, Biol Pharm Bull)
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.
Journal
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SERPINE1 (Serpin Family E Member 1)
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PAI1 expression • SERPINE1 expression
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paclitaxel • tamoxifen • cyclophosphamide • vincristine • vinblastine
over1year
MiRNA-145-5p inhibits gastric cancer progression via the serpin family E member 1- extracellular signal-regulated kinase-1/2 axis. (PubMed, World J Gastrointest Oncol)
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.
Journal
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SERPINE1 (Serpin Family E Member 1) • MIR145 (MicroRNA 145)
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PAI1 expression • SERPINE1 expression • SERPINE1 overexpression
over1year
PAI-1 mediates acquired resistance to MET-targeted therapy in non-small cell lung cancer. (PubMed, PLoS One)
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.
Preclinical • Journal
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SERPINE1 (Serpin Family E Member 1)
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MET amplification • SERPINE1 expression • SERPINE1 overexpression
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Xalkori (crizotinib)
almost2years
Therapy-induced senescent tumor cell-derived extracellular vesicles promote colorectal cancer progression through SERPINE1-mediated NF-κB p65 nuclear translocation. (PubMed, Mol Cancer)
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.
Journal • Tumor cell
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SERPINE1 (Serpin Family E Member 1) • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
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PAI1 expression • SERPINE1 expression
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irinotecan
almost2years
Serpine1 mRNA confers mesenchymal characteristics to the cell and promotes CD8+ T cells exclusion from colon adenocarcinomas. (PubMed, Cell Death Discov)
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.
Journal
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CD8 (cluster of differentiation 8) • SERPINE1 (Serpin Family E Member 1)
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CD8 expression • PAI1 expression • SERPINE1 expression