Ask about this productRelated genes to: SERPINE1 antibody
- Gene:
- SERPINE1 NIH gene
- Name:
- serpin family E member 1
- Previous symbol:
- PLANH1, PAI1
- Synonyms:
- PAI
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: SERPINE1 antibody
Related articles to: SERPINE1 antibody
- Gastrointestinal stromal tumors (GIST) can become malignant upon recurrence and metastasis, yet no drugs specifically target these processes. This study explores the effectiveness and mechanism of paeoniflorin in treating GIST. Initially, the impact of paeoniflorin on the viability, proliferation, and migration of GIST cell lines (GIST-T1 and GIST-882) was assessed using CCK-8, transwell, and wound healing assays at low (5 μM) and high (20 μM) concentrations. Subsequently, datasets GSE136755 and GSE21315 were analyzed to identify potential therapeutic targets for inhibiting GIST transfer. Key genes and pathways related to Paeoniflorin's anti-GIST effects were identified through molecular docking and Western blotting. Paeoniflorin influenced cell viability, proliferation, and migration in GIST-T1 and GIST-882 cell lines at low (5 μM) and high (20 μM) concentrations. We identified 761 differentially expressed genes (DEGs) and selected 50 hub genes using a PPI network. By screening paeoniflorin's potential targets, we identified eight key genes (CYP1A2, CYP2C9, CYP3A4, F2, ICAM1, NR1H4, PLG, and SERPINE1) that were significantly elevated in metastatic GIST samples. CYP3A4 was confirmed as a target of Paeoniflorin in GIST treatment through molecular docking and Western blotting. Pan-cancer analysis showed CYP3A4's enrichment in the tight junction pathway and a significant negative correlation with AKT2 protein. Paeoniflorin treatment led to high AKT2 expression in the tight junction pathway in GIST cell lines. Paeoniflorin acts on the CYP3A4 protein to affect the tight junction pathway, inhibiting the malignant metastasis of GIST. - Source: PubMed
Publication date: 2026/04/23
Cui DapengCui ZeyinLi YansenFan ShuangLi LeiYang ChengYu RuixiaCui JiaxinFu RunjiaFei Jiandong - The repair of critical-sized bone defects remains a significant clinical challenge due to the difficulty in achieving spatio-temporal coordination between osteogenesis and angiogenesis. This study aimed to identify key molecular regulators bridging these processes in human dental pulp stem cells (hDPSCs) and to evaluate the therapeutic efficacy of a bio-inspired delivery system comprising SERPINE1-loaded hydroxyapatite/chitosan microspheres (HA/CS MS) for vascularised bone regeneration. - Source: PubMed
Publication date: 2026/04/20
Li BangGuan RonghuaZhan ChaoningZhuo QiangqiangZhu RuiqiYan KangYang FanJin XinDu HaoranYin XuanYu RuiLu XiaoxuanLin YifanHu XiaoyanXu Jianguang - Lung adenocarcinoma is the most common histological subtype of lung cancer worldwide, yet the precise mechanisms driving its progression remain poorly understood. Methionine has been shown to promote the proliferation, migration, and invasion of lung adenocarcinoma cells. Furthermore, methionine induces the development of cancer stem cell (CSC)-like properties, which are critical for self-renewal and tumor initiation, in A549 and H460 cells. Gene expression analysis identified SERPINE1 as the primary gene upregulated in A549 cells following methionine treatment. SERPINE1, also known as serine protease inhibitor clade E member 1, functions as an inhibitor of tissue plasminogen activator and urokinase. Its involvement in the growth and progression of various cancers has been suggested. Here, we demonstrated that SERPINE1 depletion inhibited lung adenocarcinoma cell proliferation and suppressed CSC-like properties in A549 and H460 cells. This effect was reversed upon methionine supplementation. Mechanistically, the knockdown of SERPINE1 resulted in reductions in intracellular methionine, S-adenosylmethionine (SAM), and S-adenosylhomocysteine (SAH) levels in both in vitro and in vivo models, which was counteracted by the overexpression of the transcription factor BACH1. These findings suggest that a BACH1-driven SERPINE1 axis may contribute to the promotion of lung adenocarcinoma stemness by regulating methionine metabolism. - Source: PubMed
Publication date: 2026/04/17
Wen XupengHao ShengyuZhong MingJiang Pan - Hypoxia-inducible factor-1α (HIF-1α) regulates multiple pathways involved in metabolism, inflammation, and coagulation and may contribute to thrombotic complications in patients with BCR::ABL1-negative myeloproliferative neoplasms (MPN). This study investigated the expression of selected HIF-1α-regulated and thrombo-inflammatory genes (SLC2A1, F3, SELP, VEGFA, SERPINE1, PROS1, NLRP3 and THBS1) and their association with thrombotic events, JAK2 mutation status, and cytoreductive therapy. - Source: PubMed
Publication date: 2026/04/16
Morath OlgaWolfrum ThereseCrodel CarlHochhaus AndreasErnst ThomasRinke Jenny - Persistent high-risk human papillomavirus (HPV) infection, particularly types 16 and 18, is the primary driver of cervical carcinogenesis. These viruses utilize viral oncoproteins to manipulate host gene expression through multiple regulatory mechanisms. Within this landscape, microRNAs (miRNAs) emerge as critical posttranscriptional modulators that contribute to the dysregulation of pathways involved in cellular transformation and tumor progression. In this study, we investigated HPV-associated miRNA dysregulation using HPV-negative (C33A) and HPV-positive (SiHa, HeLa) cervical cancer cell lines, integrating custom microarray profiling with comprehensive systems biology and bioinformatic analyses. Our results identified 42 dysregulated miRNAs, including hsa-miR-125b-5p, hsa-miR-106b-5p, hsa-miR-23b-3p, and hsa-miR-30d-5p, which were significantly down-regulated across all experimental models. Integration of these miRNAs with cervical carcinoma transcriptomic data (GSE151666) revealed that HPV16 and HPV18 distinctly remodel host gene networks to drive malignancy. Network analysis pinpointed specific regulatory hubs, such as and for HPV16, and and for HPV18, which may facilitate malignant tumor growth by disrupting metabolic, keratinization, and extracellular matrix pathways. Furthermore, drug-gene interaction mapping highlighted potential therapeutic targets including , , and . These findings suggest that different HPV subtypes may employ unique miRNA-mediated strategies to promote cancer, offering new avenues for the development of precise diagnostic biomarkers and targeted therapies within cervical cancer research. - Source: PubMed
Publication date: 2026/04/03
Khan IshratSuneesh N SHarshithkumar RMore AshwiniNandi Shyam SundarKhan Abdul ArifMukherjee Anupam