Rabbit Polyclonal to Human TFPI_2
- Known as:
- Rabbit Polyclonal Human TFPI_2
- Catalog number:
- REF0012-1
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Agren
- Gene target:
- Rabbit Polyclonal Human TFPI_2
Related genes to: Rabbit Polyclonal to Human TFPI_2
- Gene:
- TFPI2 NIH gene
- Name:
- tissue factor pathway inhibitor 2
- Previous symbol:
- -
- Synonyms:
- PP5, TFPI-2, REF1
- Chromosome:
- 7q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-14
- Date modifiied:
- 2016-10-05
Related products to: Rabbit Polyclonal to Human TFPI_2
Related articles to: Rabbit Polyclonal to Human TFPI_2
- Immune-mediated killing triggers dynamic transcriptional adaptations in tumor cells that can reciprocally regulate the cytolytic process. Unraveling such feedback mechanisms is crucial for advancing cancer immunotherapy. Here, we identified tissue factor pathway inhibitor 2 (TFPI2) as a central node in natural killer (NK)-glioblastoma cross talk. Using transcriptomic and functional approaches, we demonstrated that NK cell attack induces TFPI2 expression in glioblastoma cells via IL1β- and TNFα-driven activation of NFκB signaling. TFPI2 not only restrains tumor proliferation by suppressing the POU2F2-CCND1 axis but also enhances NK cytotoxicity through two complementary mechanisms: It supports optimal ICAM1 expression to promote NK-tumor adhesion, and it selectively represses the immune checkpoint molecule SIGLEC15, restoring NK cell effector function. In vivo, loss of TFPI2 accelerates glioblastoma progression and abrogates the efficacy of adoptive NK cell therapy in a context-dependent manner; the functionality is likely restricted to tumors retaining the capacity for TFPI2 induction upon inflammatory stimuli. Our findings identified the TFPI2-ICAM1 and TFPI2-SIGLEC15 axes as conditional regulators of immune-tumor adhesion and checkpoint control, supporting TFPI2 as a candidate therapeutic target for a subset of glioblastomas amenable to inflammatory reprogramming. - Source: PubMed
Publication date: 2026/06/18
Zheng DongpengLi FengqiZhang ZhuangDong YunyiZhang XuebinLi XuerenYang JingyuePeng ShouchunChen BudongSun ShupengLiu ZichuanMu Xin - Tissue factor pathway inhibitor 2 (TFPI2), a serine protease inhibitor, plays a multifaceted role in tumor metastasis. Traditionally viewed as a metastasis suppressor, it inhibits extracellular matrix (ECM) remodeling, epithelial-mesenchymal transition, and angiogenesis. However, emerging evidence indicates that TFPI2 promotes tumor progression in glioblastoma, melanoma, and other cancers by fostering an immunosuppressive tumor microenvironment, mediating pathological ECM remodeling, and enhancing angiogenesis and hematogenous dissemination. Notably, even within the same metastatic cascade, TFPI2 exhibits divergent expression patterns and context-dependent opposing functions, acting either as a metastasis suppressor or promoter. This review summarizes its context-dependent regulatory mechanisms, investigates the underlying basis from structural duality, microenvironmental heterogeneity, and receptor differences, and evaluates its potential as a therapeutic target. Future research should elucidate spatiotemporal microenvironmental dynamics to support early screening and precise intervention. - Source: PubMed
Publication date: 2026/05/30
Guo ZhanliLuo YuankeWen JinyuJiang YifangKuang QixuanMa QiongZheng ChuanLi XuekeYou FengmingFu Xi - Combinations of anti-PD-1/PD-L1 immunotherapy (IO) and anti-VEGF tyrosine kinase inhibitor (TKI) are recommended as first-line therapy for metastatic renal cell carcinoma (RCC). We aimed to evaluate the predictive value of tissue factor pathway inhibitor 2 (TFPI2) for IO + TKI response. - Source: PubMed
Publication date: 2026/05/22
Wang JiajunDu LingzhiWang YingWang HangZhu YanjunXu Xianglai - Glioma stem cells (GSCs) are a small subset of self-renewing, plastic, and multipotent neoplastic cells in glioblastoma (GBM) that sit at the apex of a cellular differentiation hierarchy. Elucidating pathways that enhance GSC properties and determine their cell-specific interactions within the immunosuppressive GBM microenvironment are critical for developing effective therapeutic approaches. The CLOCK-BMAL1 complex, which is well known for its activity as a circadian rhythm-regulating transcription factor, plays a critical role in maintaining GSC stemness, and the gene encoding CLOCK was found to be amplified in about 5% of GBM cases. Here, Zhou et al. have uncovered a "symbiotic exclusivity" relationship between CLOCK-BMAL1 and TFPI2, which is also amplified in a small proportion of GBM cases. This relationship forms a HIF-1α/NF-κB P65-mediated positive feedback loop that boosts the proliferative and tumor-enhancing capacities of GSC and immunosuppressive microglia. This self-amplifying regulatory circuit represents an opportunity for intervention to inhibit GBM growth. - Source: PubMed
Publication date: 2026/05/15
Basakis PetrosShih Ling-KaiLi JiaboBrat Daniel J - Breast cancer (BC) incidence continues to rise, and recurrence and metastasis remain major contributors to mortality. The epithelial-mesenchymal transition (EMT), associated with the acquisition of invasive functions by epithelial cells, also promotes resistance to anticancer therapies. Here, an EMT-based prognostic model was developed to enhance BC outcome prediction. - Source: PubMed
Publication date: 2026/03/15
Wu ZizhengZheng JieMen ShuaiSui ShuangruiYan WeitaoLiu YinfengHan Meng