MMP14 Antibody
- Known as:
- MMP14 Antibody
- Catalog number:
- XW-7751
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- MMP14 Antibody
Related genes to: MMP14 Antibody
- 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
Related articles to: MMP14 Antibody
- Glioblastoma is the most aggressive primary brain tumor in adults and is characterized by diffuse invasion and profound remodeling of the tumor microenvironment. Tumor-associated microglia and macrophages represent the largest non-malignant population in glioblastoma and promote invasive growth through context-dependent inflammatory and matrix-remodeling programs, yet the endogenous microenvironmental cues that drive their pro-invasive activation remain incompletely defined. Tenascin-C (TNC) is an extracellular matrix glycoprotein abundantly expressed in glioblastoma and a reported endogenous ligand of Toll-like receptor 4 (TLR4). Here, we investigated whether tumor-derived TNC engages TLR4 signaling in host myeloid cells, consistent with a role to promote glioma invasion through induction of matrix metalloproteinases. To this end, we combined analyses of freshly resected human glioblastoma specimens, public bulk sequencing and CISH datasets, ex vivo GL261-organotypic brain slice cultures from wild-type and TLR4-deficient mice, and primary murine microglia cultures. TLR4 expression in human glioblastoma was enriched in CD11b tumor-associated myeloid cells and was linked to immunoregulatory rather than pro-inflammatory macrophage signatures. TNC was strongly upregulated in tumor tissue, derived predominantly from non-myeloid CD45 cells, and was spatially enriched in invasive and perivascular regions, where it was juxtaposed to reactive Iba1 microglia displaying an amoeboid morphology. Across independent glioma cohorts, TNC expression correlated with the membrane-anchored matrix-remodeling protease MMP14, particularly within anatomically defined invasive tumor compartments, and combined high TNC and MMP14 expression was associated with shorter overall survival. Functionally, host TLR4 deficiency reduced glioma growth and infiltrative expansion in organotypic brain slices, and in primary microglia, TNC induced a robust upregulation of MMP14 that was markedly attenuated in TLR4-deficient cells, whereas MMP9 regulation was modest and only partially TLR4-dependent. Cell-type-resolved single-nucleus and ligand-receptor analysis (CellChat/LIANA+) in two independent datasets (BrainTIME, GBM-CARE) further supported directional TNC-TLR4 communication from non-myeloid/malignant to myeloid populations. Together, these findings support a model in which tumor-derived TNC contributes to TLR4 activation in host myeloid cells and is associated with a pro-invasive microenvironmental program involving MMP14 induction in GBM. The identified TNC-TLR4-MMP14 signaling axis links extracellular matrix remodeling with innate immune activation, which highlights a potential tumor immune mechanism contributing to glioma invasion. - Source: PubMed
Publication date: 2026/09/08
Haneke HannahEfe Ibrahim EDzaye OmarKettenmann HelmutYalcin Fatih - We examined the associations of several reproductive factors with expression of stromal fibroblast markers αSMA, TNC, FAP, S100A6, and MMP14. - Source: PubMed
Publication date: 2026/09/22
Ratcliffe MaiseyHeng Yujing JGuzman-Arocho Yaileen DRosner BernardTamimi Rulla MYaghjyan Lusine - Ovarian cancer is the leading cause of gynecological cancer death for women in the United States. Aging and obesity are known risk factors that increase incidence rate, severity, and metastatic progression of ovarian cancer. With aging and obesity, physiological changes occur including increased inflammation, altered metabolism, and, most notably, extracellular matrix (ECM) remodeling. Remodeling of the ECM is critical for accommodating adipocyte expansion in obesity and arises from accumulated modifications with aging. The already remodeled collagen under these host factors is driven by remodeling enzymes such as matrix metalloproteinases (MMPs). Of particular interest is membrane-bound MT1-MMP, which is required for invasion in metastatic ovarian cancer. MT1-MMP is responsible for the directed collagenolysis of the ECM, which is a barrier to metastatic growth. Because of metastatic dependence on MT1-MMP, there have been many attempts to inhibit this enzyme, but current therapies lack specificity and cause significant adverse side effects. Nonetheless, novel therapeutic interventions targeting MT1-MMP are promising to improve selectivity. In this chapter, we will highlight key pathways regulating MT1-MMP expression, impact on oncogenic phenotypes, and the mechanisms that aging and obesity use to further promote ECM remodeling and accelerate disease progression, while assessing past and future challenges to study and targeting MMPs for cancer treatment. - Source: PubMed
Publication date: 2026/09/14
Strasiotto Brighton CStack Mary Sharon - 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