MMP14 ELISA kit
- Known as:
- MMP14 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-MMP14-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- MMP14 ELISA kit
Related genes to: MMP14 ELISA kit
- 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
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- Lymph node metastasis (LNM) is a major determinant of prognosis in gastric adenocarcinoma. Although lymphovascular invasion (LVI) and perineural invasion (PNI) are established markers of aggressive tumor behavior, their combined association with nodal dissemination has not been systematically evaluated. This study investigated the relationship between invasive histopathologic features and LNM and developed a composite invasion score. This retrospective study included 395 patients with gastric adenocarcinoma. Clinicopathological analyses involving LNM were performed in the surgical resection cohort. A composite invasion score (0-2) was generated based on the presence of LVI and PNI. Associations with LNM, metastatic lymph node burden, and lymph node ratio (LNR) were evaluated using non-parametric tests and multivariable logistic regression. Predictive performance was assessed using receiver operating characteristic (ROC) analysis. An exploratory external transcriptomic analysis was performed using the GSE15459 dataset. Both LVI and PNI were significantly associated with LNM (both < 0.001). The composite invasion score showed a stepwise association with nodal dissemination, with median metastatic lymph node counts increasing from 0 in score-0 tumors to 3.5 in score-1 and 9 in score-2 tumors ( < 0.001). After adjustment for pathological T stage, histological grade, Lauren classification, age, and tumor location, the composite invasion score remained an independent predictor of LNM (OR = 4.53, 95% CI: 1.81-13.00, = 0.002). LNR also increased significantly across score categories ( < 0.001). The composite invasion score demonstrated good discriminatory performance for LNM (AUC = 0.848, 95% CI: 0.773-0.923). The exploratory transcriptomic analysis demonstrated significant upregulation of , , and in advanced-stage tumors, consistent with increased extracellular matrix remodeling and stromal activation. A simple composite invasion score integrating LVI and PNI is independently associated with lymph node metastasis and metastatic burden in gastric adenocarcinoma. The accompanying exploratory transcriptomic analysis provides biological context for these clinicopathological findings by demonstrating stage-associated extracellular matrix remodeling rather than direct molecular validation of the proposed score. These findings support the potential utility of the composite invasion score as a postoperative pathology-derived risk stratification tool. - Source: PubMed
Publication date: 2026/08/22
Karcı EbruYoushanlui Mahya AhmadpourOzden FerhatAcikgoz OzgurÖlmez Ömer FatihYildiz OzcanUzun HafizeBilici Ahmet - Familial adenomatous polyposis (FAP) is a hereditary colorectal cancer (CRC). We performed genetic testing on nine FAP patients and identified a recurrent mutation at the 671st site of the MUC20 gene-MUC20-S671C. This mutation has a detection frequency of zero in the 1000 Genomes Project database. Previous studies have demonstrated that MUC20 can promote CRC progression through epithelial-mesenchymal transition (EMT). We conducted a series of experiments to analyze the impact of this mutation on CRC cells, aiming to infer its potential role and significance in CRC patients. - Source: PubMed
Publication date: 2026/07/27
Yan LiHe XinyuLi TingChen RuobingYang JunLiu Weiqing - Approximately 10% of glioblastomas harbor targetable genomic fusions. participates in a variety of fusion events that drive tumorigenesis. Two previous reports have described fusions in adult glioblastoma patients with poor survival. - Source: PubMed
Publication date: 2026/08/20
Sadanandappa Madhumala KKarbhari NishikaKnowles BrizhaPalisoul Scott MHughes Edward GTafe Laura JZanazzi George JLin Chun-ChiehHong Jennifer - Dedifferentiated liposarcoma (DDLPS) is an aggressive mesenchymal malignancy coexisting with a low grade well-differentiated component. Pathways implicated in liposarcoma growth and dedifferentiation are promoted by heparan sulfate (HS) proteoglycans (HSPG) and their modifying enzymes including heparanase. HSPGs serve as co-receptors enhancing tyrosine kinase signaling and tumor aggressiveness. Targeting these interactions bears promise in attenuating liposarcoma growth. We employed an investigational HS mimetic, the non-anticoagulant heparin CX-01 (dociparstat), to assess its HS competition impact on deregulated adipogenic differentiation and growth of human DDLPS cell lines and patient-derived xenografts (PDXs). Remarkably, CX-01 reduced colony formation and invasive capacities of DDLPS cell lines, inducing cytoskeleton remodeling, lipid accumulation and reactivation of adipogenic program. Mechanistic studies into the anti-DDLPS activity of CX-01 unveiled Syndecan 1 (SDC1)/heparanase system and receptor tyrosine kinase-AKT signaling as targets of cell growth inhibition and induction of differentiation. CX-01 treatment of mice harboring DDLPS PDXs attenuated tumor growth, enhanced lipid content and consistently altered the transcriptome, modulating pathways associated with tumor dedifferentiation (adipogenesis and fatty acid metabolism) and tumor-microenvironment interaction (TGFβ signaling, inflammatory response). In two independent cohorts of DDLPS patients, genes downregulated in CX-01-treated PDXs (SDC1, TIMP1, FN1, COL5A1, and MMP14), were found preeminently expressed in the dedifferentiated, compared to the well-differentiated tumor component and normal fat. This suggests a role for these genes in disease progression. Collectively, this study demonstrates the remarkable potential of HS competition to simultaneously block multiple anti-adipogenic players representing metabolic vulnerabilities, and to promote a differentiated tumor phenotype markedly less aggressive. - Source: PubMed
Publication date: 2026/08/11
Lanzi CinziaFavini EnricaDal Bo LauraTortoreto MonicaPercio StefanoZuco ValentinaDagrada Gian PaoloBrich SilviaCollini PaolaDe Cecco LorisCallegaro DarioSanfilippo RobertaGronchi AlessandroZaffaroni NadiaAssaraf Yehuda GPasquali SandroCassinelli Giuliana - Vitamin D has been reported to act as a tissue-protective regulator by suppressing Matrix Metalloproteinases (MMPs) and upregulating Tissue Inhibitors of Metalloproteinases (TIMPs), though changes may be body mass index (BMI)-dependent; however, the relationship between vitamin D metabolism and matrix remodeling pathways in Polyendocrine Metabolic Ovarian Syndrome (PMOS) remains poorly understood. In women with PMOS ( = 28) and controls ( = 28), 12 MMPs and 3 TIMPs were determined by Slow Off-rate Modified Aptamer (SOMA)-scan plasma protein measurement and correlated to 25-hydroxyvitamin D (25(OH)D) and its metabolites (active 1,25-dihydroxyvitamin D (1,25(OH)D) and 24,25-dihydroxyvitamin D (24,25(OH)D)) measured by gold standard isotope-dilution liquid chromatography tandem mass spectrometry. Insulin resistance and systemic inflammation (normal C-reactive protein) were comparable between PMOS and control women, though PMOS had higher free androgen index and anti-Mullerian hormone levels. Vitamin D and its metabolites did not differ between groups. Only MMP16 was lower in PMOS than controls (549.6 ± 58.3 vs. 678.0 ± 304.1 Relative Fluorescent Units, = 0.037) but did not pass the false discovery rate. In women with PMOS, 25(OH)D and 24,25(OH)D demonstrated significant inverse correlations with TIMP3 (r = -0.60, = 0.005 and r = -0.58, = 0.007, respectively). Multivariable regression confirmed independent inverse associations between TIMP3 and both 25(OH)D (β = -51.1, = 0.031) and 24,25(OH)D (β = -858.7, = 0.028) after adjustment for age, body mass index and Homeostatic Model Assessment-Insulin Resistance, and the association remained stable following bootstrap internal validation. Additional moderate associations were observed between vitamin D metabolites and membrane-type MMPs (MMP14, MMP16, MMP17). Exploratory analyses suggested potential inverse associations between vitamin D metabolites and TIMP3, together with weaker associations involving MMP14, MMP16 and MMP17, suggesting the novel hypothesis that vitamin D may influence extracellular matrix remodeling and ovarian stromal biology through regulation of TIMP3-dependent pathways independently of obesity and insulin resistance, rather than through MMPs directly. - Source: PubMed
Publication date: 2026/07/24
Zainalabedin MashaelSmahi NoraSathyapalan ThozhukatButler Alexandra EAtkin Stephen L