MMP14 antibody (FITC) Polyclonal Antibodies Primary antibodies
- Known as:
- MMP14 (anti-) (fluorecein) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb15995
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- MMP14 antibody (FITC) Polyclonal Antibodies Primary antibodies
Related genes to: MMP14 antibody (FITC) Polyclonal Antibodies Primary antibodies
- Gene:
- MMP14 NIH gene
- Name:
- matrix metallopeptidase 14
- Previous symbol:
- -
- Synonyms:
- MT1-MMP
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-20
- Date modifiied:
- 2016-10-05
Related products to: MMP14 antibody (FITC) Polyclonal Antibodies Primary antibodies
Related articles to: MMP14 antibody (FITC) Polyclonal Antibodies Primary antibodies
- Emerging evidence suggests that perturbation of TGF-β signaling in parenchymal cells drives malignant transformation and cancer progression in a subset of patients with primary liver cancer (PLC). TGF-β plays a crucial role in liver pathophysiology with diverse effects on various processes and cell types. In liver homeostasis, TGF-β signaling exerts tumor-suppressive functions that are often lost during carcinogenic transformation, when downstream signaling rebranches from tumor-suppressive to pro-tumorigenic, facilitating invasiveness and metastasis. In this study, primary patient-derived and established liver cancer cell lines were exposed to TGF-β1 and TGF-β2, and effects on tumor-initiating potential, invasion, and migration were assessed by in vitro analyses including colony/sphere formation and wound healing assays. RNA sequencing and reverse-phase protein array (RPPA) were employed to analyze differential gene and protein expression across treatments. Our findings demonstrate that TGF-β1 and TGF-β2 reduced proliferation, colony and spheroid formation in investigated cell lines. Notably, TGF-β1 increased migratory and invasive properties of both HCC and CCA cell lines, whereas TGF-β2 had no such effect. Transcriptome profiling revealed activation of gene sets associated with cell cycle regulation by both ligands. Pro-migratory effects of TGF-β1 were linked to epithelial-mesenchymal transition (EMT), including enrichment of matrix metalloproteinase (MMP) and actin cytoskeleton pathways. Specifically, TGF-β1 downregulated epithelial marker E-cadherin and upregulated mesenchymal markers Vimentin and SNAIL. RPPA indicated p21 induction by both ligands, causing cell cycle arrest, while TGF-β1 specifically upregulated MMP14, promoting EMT-related properties. In conclusion, targeting TGF-β1-MMP14-EMT pathway could complement TGF-β-based therapies in PLC management. - Source: PubMed
Publication date: 2026/06/03
Castven DarkoPereira SharonRodriguez Luis ZFischer Merle EMarini FedericoDooley StevenSalié Henrikevon Felden JohannJegodzinski LinaMeindl-Beinker Nadja MLee Ju-SeogGalle Peter RMarquardt Jens U - Longitudinal monitoring of tumor progression and metastasis provides significant benefits to improve the treatment outcome of breast cancer. Matrix metalloproteinase 14 (MMP14) on extracellular vesicles (EVs) is highly relevant to tumor invasiveness, yet the sensitivity and specificity of detection are hindered by tremendous amounts of normal EVs amidst complex blood samples. Here we developed an ultrafast one-step dual-target orthogonal barcoding-based microscale thermophoretic extracellular vesicle (DOT-EV) assay to evaluate MMP14 levels on tumor-derived EVs (T-EVs). Leveraging the orthogonal barcoding of two allosteric aptamer probes targeting MMP14 and EpCAM, our assay specifically recognizes signals from MMP14 of tumor EVs and enhances the accuracy of clinical diagnosis. The microscale thermophoresis induces convection flow and accelerates DNA assembly on EVs, enabling ultrafast one-step detection of T-EV MMP14 within just 20 s, consuming 10 μL plasma samples. The T-EV MMP14 profiling on metastatic mouse models and patient samples of breast cancer demonstrated that the DOT-EV assay can monitor different development stages of the tumor and predict metastatic potential. Notably, triple-negative breast cancer was successfully differentiated from other subtypes. The DOT-EV assay offers a pioneering tool for noninvasive and precise diagnosis, progression monitoring, and metastasis prediction of cancer, showing great promise in advancing the clinical implementation of precision medicine. - Source: PubMed
Publication date: 2026/06/03
Chen AipengWang RuokeZou YanDing YueTian RuitingWang YuqingLan FangzhouWu QiaoyiZhang PengFang XiaoniYang Chaoyong - Vascular calcification is an actively regulated process driven by vascular smooth muscle cell (VSMC) osteogenic reprogramming and promoted by oxidative stress and extracellular matrix remodeling. We investigated whether the novel histone deacetylase inhibitor YAK577 mitigates calcification by modulating an MMP14-NOX2/ROS-associated pathway in calcification medium (CM)-treated VSMCs and a vitamin D-induced arterial calcification model in 8-week-old male C57BL/6N mice. Calcification was assessed by Alizarin Red S/von Kossa staining and calcium quantification; osteogenic markers (BMP2, RUNX2, MSX2) and MMPs were examined by qRT-PCR and immunoblotting; intracellular ROS was measured by DHE staining with N-acetylcysteine as an antioxidant control; and MMP14 was manipulated by siRNA knockdown or plasmid overexpression. YAK577 was non-cytotoxic at effective concentrations and reduced CM-induced calcium deposition and osteogenic marker expression. YAK577 reduced MMP14 expression and suppressed CM-induced NOX2/p47phox activation and ROS accumulation, while GSK2795039 attenuated CM-induced DHE fluorescence. MMP14 silencing attenuated, whereas MMP14 overexpression enhanced, osteogenic signaling and increased NOX2. In vivo, YAK577 reduced vitamin D-induced aortic calcium burden, histological calcification, and the expression of MMP14, NOX2, and osteogenic markers. These data support a working model in which YAK577 alleviates vascular calcification, at least in part, by suppressing an MMP14-associated NOX2/p47phox-ROS axis. - Source: PubMed
Publication date: 2026/05/10
Zhou HongyanKee Hae JinJeong Seong MinBai LiyanWan LeKim Seong HoonLee Seung HunKurz ThomasSim Doo SunJeong Myung HoHong Young Joon - Periodontitis represents a chronic inflammatory disease resulting from the interaction between plaque-associated microorganisms and the host immune response. PANoptosis, a newly recognized programmed cell death, is linked to multiple inflammatory disorders. However, its role in periodontitis pathogenesis and diagnostic potential remains unclear. This study aimed to identify key PANoptosis-related biomarkers in periodontitis using bioinformatics analysis followed by experimental verification. - Source: PubMed
Publication date: 2026/05/15
Xi HualeiXu WanqiuLin SongYao LihongPiao GuiyanLiu YingGuo JinrongWang ShuminXie JiaxinWang Xiumei - Chronic periodontitis (CP) and postmenopausal osteoporosis (PMOP) are prevalent chronic inflammatory diseases characterized by bone resorption; however, the shared molecular mechanisms between them remain unclear. Hub genes associated with CP and PMOP were identified through bioinformatics analysis. Lipopolysaccharide (LPS)-stimulated MC3T3-E1 osteoblasts were used to establish an in vitro model, followed by lentiviral-mediated matrix metalloproteinase 14 (MMP14) knockdown. Cell viability and apoptosis were assessed using the Cell Counting Kit-8 assay and flow cytometry, respectively. Levels of inflammatory cytokines and oxidative stress markers were measured by enzyme-linked immunosorbent assay. Intracellular ROS were detected using 2',7'-dichlorodihydrofluorescein diacetate fluorescence staining. Western blot analysis was performed to assess the expression of osteoclast-related markers. The involvement of the JAK2/STAT3 pathway was assessed using the JAK2 agonist RO8191 and inhibitor AG490. PDGFRB, MMP14, VWF, PECAM1, FLT1, and CXCR4 were identified as hub genes and were all upregulated in LPS-stimulated MC3T3-E1 osteoblasts. Silencing MMP14 improved cell viability and reduced apoptosis, inflammatory cytokine release (TNF-α, IL-1β, and IL-6), oxidative stress markers (MDA and ROS), and osteoclast-associated markers (CTX-I, TRAP, and Cathepsin K), while restoring SOD activity. Mechanistically, MMP14 silencing decreased the phosphorylation levels of JAK2 and STAT3. The protective phenotype caused by MMP14 silencing was significantly abolished by RO8191 but mimicked by treatment with AG490. MMP14 may represent a potential molecular link between CP-associated bone loss and PMOP. Modulation of the MMP14-JAK2/STAT3 signaling axis may represent a promising research direction for inflammation-related bone loss. - Source: PubMed
Jiang XiliangJia WeiqiMa QinciFan WanpengLuo Shigao