PAI1 antibody
- Known as:
- PAI1 (anti-)
- Catalog number:
- 10-1940
- Product Quantity:
- 200 ul
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- PAI1 antibody
Related genes to: PAI1 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: PAI1 antibody
Related articles to: PAI1 antibody
- Metastatic breast cancer, particularly triple-negative breast cancer (TNBC), remains a major clinical challenge due to its aggressive behavior and limited therapeutic options. The molecular pathways that drive tumor progression while simultaneously promoting immune evasion are not well defined. Here, we identify S100A7/RAGE signaling as a central oncogenic and immunomodulatory axis that drives TNBC tumorigenicity, metastasis, and immune suppression. In this study, we have shown that S100A7/RAGE signaling plays a vital role in driving invasive TNBC tumorigenicity by activating Stat3 and elevating Serpin-E1 expression. Furthermore, we revealed that combinatorial treatment of Stat3 and RAGE inhibitors synergistically inhibits the tumorigenicity of S100A7-expressing TNBC cells in-vitro by suppressing AKT/MAPK signaling and mitigates the tumor burden, especially distant metastasis in-vivo using TNBC cell lines and a conditional mammary gland-specific S100A7 overexpression bitransgenic mouse model. Moreover, our study also shed light on the dynamic interplay between the S100A7/RAGE/Stat3 signaling pathway and immune cell infiltration within the tumor microenvironment. Remarkably, our findings underscored the potential of combined inhibition to enhance anti-tumor immune responses, fostering the infiltration of anti-tumor MHCII and iNOS macrophages and activated effector CD8 tumor-infiltrating T cells. Moreover, CD8 T cells depletion abrogates the therapeutic benefits of RAGE/Stat3 inhibition by restoring the tumor growth in S100A7 overexpression mice. Importantly, we discovered that S100A7/RAGE signaling modulates anti-tumor macrophage phenotypes by regulating Serpin-E1 expression on TNBC cells. S100A7 regulates Serpin-E1 gene expression by enhancing the direct binding of pStat3 (Ser727) to its promoter. Notably, neutralization of Serpin-E1 in combination with RAGE and Stat3 inhibition increased iNOS expression in macrophages in-vitro and significantly enhanced overall anti-metastatic efficacy in-vivo. Importantly, we found that increased co-expression of S100A7 and Serpin-E1 correlated with worse prognoses in TNBC patients, whereas the presence of iNOS or MHCII genes improved the overall prognosis, especially basal and immunomodulatory subtypes, which also underscores the clinical relevance of targeting these signaling molecules as a promising translational therapeutic strategy for TNBC. Overall, these findings provide new avenues for therapeutic interventions in metastatic TNBC. - Source: PubMed
Publication date: 2026/04/29
Ghanta PratyushaVerma Ajeet KLin Cho-HaoCharan ManishKoshre Ganesh RAgarwal ShashwatAdorno JonathanGarg Ayush ArpitMukherjee TanishaMiles Wayne OSong Jonathan WMishra SanjayGanju Ramesh K - - Source: PubMed
Publication date: 2026/03/31
Lu Thu Ngoc AnhHiggins Paul - Plasminogen activator inhibitor-1 (PAI-1) plays a key role in modulating fibrinolysis. However, its role in the thrombotic autoimmune disease known as antiphospholipid syndrome (APS) remains understudied. - Source: PubMed
Publication date: 2026/04/27
Gan YuzhouLiang WenyingLiu ChaoYalavarthi SrilakshmiWarnock MarkSabb KaitlynSarosh CyrusSchaefer Jordan KTambralli AjayMadison Jacqueline AEmal Cory DTsou Pei-SuenShi HuiZuo YuLawrence Daniel AKnight Jason S - 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