Ask about this productRelated genes to: TFPI Blocking Peptide
- Gene:
- TFPI NIH gene
- Name:
- tissue factor pathway inhibitor
- Previous symbol:
- LACI
- Synonyms:
- EPI, TFI, TFPI1
- Chromosome:
- 2q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-03
- Date modifiied:
- 2016-10-05
- 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: TFPI Blocking Peptide
Related articles to: TFPI Blocking Peptide
- Colorectal cancer (CRC) is a major global malignancy, with ferroptosis emerging as a key regulator of its progression. Although TFPI-2, a kunitz-type serine protease inhibitor, was reported to have important clinical implications for CRC diagnosis and prognosis, few studies have investigated its functional role in CRC cells, and its involvement in ferroptosis remains unknown. TFPI-2 expression in CRC and adjacent normal tissues was detected by IHC, RT-qPCR, and Western blot. Plasmid transfection was used to silence or overexpress TFPI-2 in CRC cells, followed by functional assays including CCK-8 assays, EdU staining, Transwell assays, and EMT marker detection. In vivo tumor growth was evaluated using a xenograft model. Ferroptosis was assessed by measuring ROS, Fe²⁺ levels, MDA, GSH, and expression of key regulators (GPX4, TFR1, FSP1). Mechanistic insights from analyses of p65 and IκBα were obtained through RT-qPCR, Western blot and immunofluorescence. To investigate the involvement of the NF-κB signaling pathway, HCT116 cells were treated with the NF-κB inhibitor Bay 11-7082. CRC tissues exhibited decreased TFPI-2 expression. Overexpressing TFPI-2 suppressed CRC cell proliferation, invasion, and EMT, whereas TFPI-2 knockdown exacerbated these malignant phenotypes. These findings were further validated in xenograft models, where TFPI-2 exerted tumor-suppressive effects. Mechanistically, TFPI-2 knockdown inhibited ferroptosis by promoting NF-κB pathway activity. This study reveals that TFPI-2 suppresses CRC progression by inducing ferroptosis through NF-κB signaling, providing new insights for future CRC therapy. - Source: PubMed
Shi XiaojingZhang JingLu JianQiXu Zheng - - Source: PubMed
Publication date: 2025/09/17
Wang GuangliHuang WenheLi WeiChen ShaoyingChen WeibinZhou YanchunPeng PeiGu Wei - Bone and bone-marrow (BM) have the same blood supply and thus may be considered as one organ. We previously demonstrated that the microcirculation hemostatic balance that includes heparanase, tissue factor (TF), TF pathway inhibitor (TFPI) and TFPI-2 are organ dependent. The present study aim was to investigate the effect of BM microcirculation blood on osteoblasts and human umbilical vein endothelial cells (HUVECs) compared with peripheral-blood (PB). Fourteen patients were recruited. BM blood was drawn from the pelvis and PB from the arm of each patient. Mesenchymal stem cells (MSCs) from the bone pellet were differentiated to osteoblasts. Cells were evaluated by ELISA, chromogenic assays and immunostaining. We found that levels of heparanase, TF, TFPI, and TFPI-2 were reduced in osteoblasts compared with MSCs (p < 0.05). Level of heparanase was lower in BM plasma compared with PB (p < 0.05). BM plasma attenuated heparanase procoagulant activity and level and increased proliferation in osteoblasts and HUVECs compared to PB plasma or the control. BM plasma increased HUVECs tube-formation compared with PB and control. Peptide 16AC, derived from heparanase that interacts with TF, enhanced, while peptide 6, that inhibits the interaction of heparanase-TF-complex, decreased heparanase level, procoagulant activity, and proliferation in osteoblast and HUVECs. In conclusion, osteoblasts acquire an attenuated hemostatic characteristic during differentiation. The microcirculation blood of the bone supports low hemostatic parameters in osteoblasts and enhances proliferation of cells and angiogenesis. The present data support the growing notion that the local microcirculation within a tissue or organ uniquely affects local hemostasis and angiogenesis. - Source: PubMed
Publication date: 2025/04/21
Asayag KerenPeled EliCrispel YonatanYanovich ChenCohen HaimKeren-Politansky AnatNadir Yona - - Source: PubMed
Konduri Santhi DRao Chilukuri NChandrasekar NirmalaTasiou AnastasiaMohanam SanjeevaKin YoshiakiLakka Sajani SDinh DzungOlivero William CGujrati MeenaFoster Donald CKisiel WalterRao Jasti S - Bone metastasis and steroids are known to activate the coagulation system and induce osteoporosis, pathological bone fractures, and bone pain. Heparanase is a protein known to enhance the hemostatic system and to promote angiogenesis, metastasis, and inflammation. The objective of the present study was to evaluate the effects of steroids and malignancy on the coagulation factors and osteoblast activity in the bone tissue. The effects of dexacort and malignant medium were evaluated in osteoblasts derived from human bone marrow mesenchymal stem cells and human umbilical vein endothelial cells (HUVECs). The bones of mice treated with dexacort for 1 month were studied. Bone biopsies of ten patients with bone metastasis, ten with steroid-induced avascular necrosis (AVN), and ten with osteoarthritis were compared to ten controls. We found that dexacort and malignant medium significantly increased the heparanase levels in osteoblasts and HUVECs and decreased the levels of alkaline phosphatase (ALKP). Peptide 16AC, derived from heparanase, which interacts with tissue factor (TF), further increased the effect, while peptide 6, which inhibits interactions between heparanase and TF, reversed the effect in these cells. The bone microcirculation of mice treated with dexacort exhibited significantly higher levels of heparanase, TF, TF pathway inhibitor (TFPI), TFPI-2, thrombin, and syndecan-1, but reduced levels of osteocalcin and ALKP. The pathological human bone biopsies' microcirculation exhibited significantly dilated blood vessels and higher levels of heparanase, TF, TFPI, TFPI-2, and fibrin. In summary, steroids and malignancy increased the activation of the coagulation system in the bone microcirculation and reduced the osteoblast activity. Heparanase inhibitors should be further investigated to attenuate bone fractures and pain. - Source: PubMed
Publication date: 2024/11/26
Asayag KerenPeled EliAssalia MaiCrispel YonatanYanovich ChenCohen HaimKeren-Politansky AnatNadir Yona