ADAM15
- Known as:
- ADAM15
- Catalog number:
- ARP46370_P050
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- ADAM15
Related genes to: ADAM15
- Gene:
- ADAM15 NIH gene
- Name:
- ADAM metallopeptidase domain 15
- Previous symbol:
- -
- Synonyms:
- MDC15
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-01
- Date modifiied:
- 2015-08-24
Related products to: ADAM15
Related articles to: ADAM15
- A disintegrin and metalloproteinase 15 (ADAM15) is a cell-surface protease with a paradoxical role in cancer development. In this review, we provide a comprehensive overview of the dual functions of ADAM15, highlighting recent mechanisms including exosomal communication, non-coding (nc)RNA regulation (miR-3174, miR-526b-5p, and lncRNA NCK1-AS1), and antiangiogenic metargidin peptide (AMEP), which has completed Phase I trials. We also present a systematic therapeutic strategy matrix covering small molecules, antibodies, RNA therapeutics, proteolysis-targeting chimeras (PROTACs), G-quadruplex stabilizers, and combination therapies, alongside a detailed research gap analysis and actionable future directions. - Source: PubMed
Publication date: 2026/07/21
El-Far AliSong BinghuiFu JunjiangCheng Jingliang - Emerging evidence shows that morning chronotype is associated with a reduced risk of breast cancer, yet biological mechanisms remain unclear. This study aimed to identify circulating proteins that mediate this association. - Source: PubMed
Publication date: 2026/06/20
Luo ShanAi YujieZheng JieWan Eric Yuk FaiYoshiji SatoshiAu Yeung Shiu Lun - Hepatocellular carcinoma (HCC) continues to pose a major health concern for global public health, characterized by pronounced clinical heterogeneity in survival outcomes and therapeutic efficacies. The stromal senescence constitutes a major impediment in constructing robust prognostic models. This study aimed to develop and validate a robust prognostic prediction model to accurately assess the prognostic risk of HCC patients and facilitate personalized precision treatment. - Source: PubMed
Publication date: 2026/05/27
Lu JinZhang ZhenhuaYuan WeiZhang Yingjian - : Traditional breast cancer prognostic tools relying on clinical staging often miss molecular heterogeneity, leading to divergent patient outcomes. Extracellular matrix (ECM) remodeling, driven by the Matrix Metalloproteinase (MMP), ADAM, and ADAMTS enzyme families, is critical to tumor progression. This study evaluates whether integrating ECM protease transcript abundance with standard clinical variables improves survival prediction accuracy and personalized risk stratification. : Clinical and transcriptomic data from The Cancer Genome Atlas (TCGA) breast cancer cohort were analyzed. We integrated the protein-coding transcripts per million (pTPM) of top-ranked protease genes with standard clinical covariates (age, ordinal stage). Cox Proportional Hazards (CoxPH), penalized Cox (CoxNet), Random Survival Forest (RSF), and Gradient Boosting Survival (GBS) models were evaluated under a stratified 70/30 train-test split, followed by five-fold cross-validation. The locked final RSF model was then externally tested in METABRIC without retraining or risk-cutoff optimization. : Univariate screening identified ADAM15, MMP15, and ADAMTSL1 as global risk factors, whereas ADAMTS8 and MMP7 were protective. Prognostic signals were subtype-dependent. Integrated multivariable models outperformed transcript-only approaches in internal testing. The integrative RSF achieved the highest held-out discrimination (C-index = 0.797), outperforming a clinical-only Cox baseline trained on age and stage alone (C-index = 0.742, 95% CI 0.636-0.826). In METABRIC, the external C-index was 0.581 (95% CI 0.562-0.598), with significant survival separation across training-defined risk groups (log-rank < 0.0001). : ECM protease transcript profiles provide complementary prognostic information in TCGA-BRCA and show partial transportability to METABRIC. However, the modest external C-index indicates limited individual-level discrimination across platforms, so these candidate markers should be interpreted as hypothesis-generating and require further validation before clinical implementation. - Source: PubMed
Publication date: 2026/05/07
Babas RamiVynios Demitrios HKompothrekas AristotelisBoutsinas BasilisKaramanos Nikos - ADAM15, as a member of the membrane-bound protease family, participates prominently in the progression and metastasis of various tumours. However, its mechanism of action in hepatocellular carcinoma remains unclear. The functional role of ADAM15 in hepatocellular carcinoma (HCC) was investigated both in vitro and in vivo. ADAM15 knockdown inhibited the proliferation, migration and invasion of HCC cells, whereas ADAM15 overexpression enhanced these malignant behaviors. The results of apoptosis assay showed that inhibition of ADAM15 expression promoted apoptosis of HCC cells, and overexpression of ADAM15 inhibited apoptosis of HCC cells. Western Blot results showed that ADAM15 knockdown inhibited EMT transition and decreased the expression of mesenchymal marker N-cadherin. Additionally, ADAM15 silencing increased the expression of the pro-apoptotic protein Bax while decreasing the anti-apoptotic protein Bcl-2. The results of subcutaneous tumor formation assay in nude mice showed that knockdown of ADAM15 expression significantly inhibited the growth of subcutaneous tumors. The results of tail vein lung metastasis assay showed that ADAM15 knockdown inhibited lung metastasis of hepatocellular carcinoma in nude mice. In the mechanistic study, overexpression of ADAM15 activated the JNK-p38MAPK pathway, thereby promoting EMT and suppressing apoptosis in HCC cells. Conversely, ADAM15 knockdown inhibited the JNK-p38 MAPK pathway, leading to enhanced apoptosis and suppressed EMT. ADAM15 is highly expressed in hepatocellular carcinoma. ADAM15 regulates the apoptosis and EMT of hepatocellular carcinoma cells by activating the JNK-p38 MAPK signaling pathway, thereby promoting the progression and metastasis of hepatocellular carcinoma. - Source: PubMed
Publication date: 2026/04/15
Junhui XuMengyun Su