Ask about this productRelated 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
- Neutralizing sclerostin antibodies (Scl-Ab) mitigate bone loss and promote bone formation to address fracture risk in postmenopausal osteoporosis. Clinically, this treatment is administered monthly for women at high risk of fragility fractures, who are often years into menopause. Preclinical studies have demonstrated that dampening of bone formation occurs with continuous dosing at supraphysiological doses. Osteoporotic bone loss occurs rapidly during early menopause, followed by longer-term changes in bone mineralization and osteocyte activity. Whether earlier administration of lower-exposure Scl-Ab can mitigate bone loss and osteocyte-mediated mineralization is unknown. The objective of this study was to evaluate the effects of early intermittent low-dose Scl-Ab on: (1) osteoclastogenesis and bone resorption, (2) perilacunar remodelling, (3) secondary mineralization, and (4) osteocyte mechanosensitivity. Female retired breeder Wistar rats underwent bilateral ovariectomy and received monthly low-dose Scl-Ab injections (2 mg/kg/month) from 3 to 14 weeks post-OVX, while a control group remained untreated. Early intermittent low-dose Scl-Ab treatment increased bone formation and reduced osteoclastogenesis and catabolic gene expression ((Sost, Ctsk, Mmp9) compared to untreated rats. Treatment also decreased the percentage of empty lacunae and the number of MMP14+ osteocytes, accompanied by lower perilacunar mineral density and smaller lacunar size, indicating improved osteocyte survival and reduced perilacunar remodelling. Conversely, expression of osteocyte-mediated mineralization genes (DMP1, PHEX, OPN, ALP) and mechanotransduction-related genes (Vcl, integrins α5, αV, β1, CX43, Axin2, IFT88, Adcy6, Pkd1, Cav1) were reduced. Together, these findings suggest that early intermittent low-dose Scl-Ab therapy promotes surface bone formation while attenuating osteocyte-mediated mineralization after initial bone loss. - Source: PubMed
Publication date: 2026/04/07
Naqvi Syeda MasoomaAli WahaajAllison HollieO'Sullivan Laura MHoldsworth GillPanadero-Perez Juan AlbertoSchiavi-Tritz JessicaMcNamara Laoise M - Non-small cell lung cancer (NSCLC) is the most common type of lung cancer and a major contributor to cancer-related deaths globally. The mechanisms of NSCLC metastasis, largely driven by epithelial-mesenchymal transition (EMT), remain incompletely understood. The Cancer Genome Atlas - Lung Adenocarcinoma (TCGA-LUAD) dataset analysis revealed that suppression of tumorigenicity 7 (ST7) may play a role in preventing the EMT process and metastasis in NSCLC. In this study, we revealed that ST7 suppressed the expression of Matrix metalloproteinase 14 (MMP14) by binding Y-box binding protein 1 (YBX1) and blocking its nuclear translocation. Consequently, ST7 silencing enhanced both EMT and metastatic progression in NSCLC experimental models, including A549 and H1299 cell lines in vitro and a tail-vein lung metastasis model in BALB/c nude mice in vivo. Collectively, our results revealed a novel ST7/YBX1/MMP14 signaling axis that might be targeted in NSCLC metastasis. - Source: PubMed
Publication date: 2026/04/21
Qin YangChen YahanCao QianZhang BinWan Yulei - Vasculogenic mimicry (VM) is a phenomenon in which tumor cells form capillary-like networks without endothelial cells and is associated with tumor progression and poor prognosis. Understanding mechanisms of VM and identifying its reliable biomarkers are critical for developing novel therapeutic strategies. Matrix metalloproteinases (MMPs), which degrade extracellular matrix (ECM) components, have been reported to regulate VM. Indeed, increased expression of MMPs has been reported in VM-positive patients; however, their precise roles in VM formation remain unclear. Therefore, in this study, we investigated the roles of MMPs, particularly MMP2, MMP9, and MMP14, in VM formation and assessed their potential as VM markers. Expression levels of MMP2 and MMP9 in multiple types of cancer cell lines did not correlate with VM-forming ability, and knockout of either gene in HT1080 cells had no significant effect on VM formation. In contrast, MMP14 expression showed a positive correlation with VM formation, although VM structures were still maintained in MMP14-knockout MDA-MB-231 cells. Additionally, treatment with GM6001, a broad-spectrum MMPs inhibitor, had no significant impact on VM formation. Moreover, co-treatment with various known anticancer agents and GM6001 did not synergistically suppress VM. These findings suggest that MMPs inhibition does not give a vulnerability in VM formation. Collectively, our results indicate that MMPs, particularly MMP2, MMP9, and MMP14, are unlikely to play critical roles in VM formation. - Source: PubMed
Publication date: 2026/04/15
Yoshida TomokiFukuoka EmuKawahara RyotaMatsubara TeruhikoSimizu Siro - Acute kidney injury (AKI) represents a critical complication in patients with acute coronary syndrome (ACS), particularly in patients undergoing percutaneous coronary intervention (PCI). Current tests for detecting early AKI, such as creatinine and cystatin C, have modest sensitivity. This study explores the role of bioinformatics in creating an implementable predictive key gene in cardiorenal pathogenesis and evaluates the diagnostic potential of ,, and in predicting AKI in ACS patients. - Source: PubMed
Publication date: 2026/04/14
Khaled RadwaEl-Zayat EmadRagheb Mohamed AAbdelrahman Sara ElsayedMatboli Marwa - Invasion plasticity allows malignant cells to toggle between collective, mesenchymal, and amoeboid phenotypes while traversing extracellular matrix (ECM) barriers. Current dogma holds that collective and mesenchymal invasion programs trigger the mobilization of proteinases that digest structural barriers dominated by type I collagen, while amoeboid activity allows cancer cells to marshal mechanical forces to traverse tissues independently of ECM proteolysis. Here, we use cancer spheroid-3-dimensional matrix models, single-cell RNA sequencing, and human tissue explants to identify the mechanisms controlling mesenchymal versus amoeboid invasion. Unexpectedly, collective/mesenchymal- and amoeboid-type invasion programs-though distinct-are each characterized by active tunneling through ECM barriers, with expression of matrix-degradative metalloproteinases. CRISPR/Cas9-mediated targeting of a single membrane-anchored collagenase, MMP14/MT1-MMP, ablates tissue-invasive activity while coregulating cancer cell transcriptional programs. Though changes in matrix architecture, nuclear rigidity, and metabolic stress as well as the presence of cancer-associated fibroblasts are proposed to support amoeboid activity, none of these changes restore invasive activity of MMP14-targeted cancer cells. While a requirement for MMP14 is bypassed in low-density collagen hydrogels, invasion by the proteinase-deleted cells is associated with nuclear envelope and DNA damage, highlighting a proteolytic requirement for maintaining nuclear integrity. Nevertheless, when cancer cells confront explants of live human breast tissue, MMP14 is again required to support invasive activity. Corroborating these results, spatial transcriptomic and immunohistological analyses of human breast cancers identified MMP14 expression in tissue-infiltrating carcinoma cells that were further juxtaposed with proteolyzed type I collagen fragments, underlining the pathophysiologic importance of this proteinase in directing invasive activity in vivo. - Source: PubMed
Publication date: 2026/04/10
Olson Adam WLi JonathanLi Xiao-YanKing LanaJiang LongBanerjee KalinsMcCoy Atticus JGondal Mahnoor NChinnaiyan Arul MEl-Ashry DorrayaKeller Evan TPutnam Andrew JWeiss Stephen J