Human ADAM15 ProteinVector: CHO
- Known as:
- Human ADAM15 ProteinVector: CHO
- Catalog number:
- 10330-H01C
- Product Quantity:
- 20μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human ADAM15 ProteinVector: CHO
Related genes to: Human ADAM15 ProteinVector: CHO
- 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: Human ADAM15 ProteinVector: CHO
Related articles to: Human ADAM15 ProteinVector: CHO
- 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 - Colorectal cancer (CRC) remains a major global health challenge, primarily due to late-stage diagnosis and high metastatic potential. Effective management requires novel diagnostic and prognostic strategies, with a growing focus on molecular biomarkers. A Disintegrin and Metalloproteinase (ADAM) proteins, characterized by unique proteolytic activity, play a fundamental role in tumorigenesis by regulating tumor growth, epithelial-mesenchymal transition (EMT), and metastasis. Based on recent investigations, among all ADAMs, ADAM8, ADAM9, ADAM12, ADAM15, and ADAM17 have been proved to play an important role in the CRC pathogenesis. Thus, this review underscores the potential of selected ADAM family members as promising candidates for biomarkers of CRC. Elevated ADAM8, ADAM9, ADAM12 and ADAM17 levels were observed in CRC tissues and correlated with more advanced tumor stage, while increased serum ADAM15 concentrations associated with the presence distant metastases. Moreover, ADAM9, ADAM12, ADAM15 and ADAM17 levels were associated with poorer survival, whereas ADAM8 overexpression was found to be independent prognostic factor for CRC patients' survival. In addition, the measurement of serum ADAM15 concentrations, especially in combination with well-established tumor marker-CEA improved the diagnosis of patients with this malignancy. In conclusion, selected ADAM are critical contributors to the development and progression of CRC, affecting tumor growth, EMT, and metastasis. ADAM8, ADAM9, ADAM12, ADAM15 and ADAM17 were identified as promising biomarkers for the assessment of CRC progression and proved to be prognostic indicators for patients' survival. Further validation through large prospective studies and standardized assays is necessary to establish their potential in clinical practice. - Source: PubMed
Publication date: 2026/04/01
Romanowicz AdriannaŁukaszewicz-Zając MartaMroczko Barbara - Although tissue inhibitors of metalloproteinases (TIMPs) are key regulators in breast cancer, their differential expression, clinical relevance, and molecular roles remain unclear. This study aimed to compare the expression patterns of the four TIMPs in breast cancer and evaluate their molecular interactions and associated pathways through an integrated bioinformatic analysis. The expression of TIMPs and their correlations with MMPs were analyzed using the TCGA PanCancer, cBioPortal, and GEO datasets. Associations between TIMP expression and overall survival were assessed in the TCGA Breast Invasive Carcinoma PanCancer cohort. Pathway enrichment analysis was performed using GO, KEGG, and DAVID. The relationships between immune cell infiltration, stromal cells, and TIMP expression were assessed using the EPIC algorithm. Statistical analyses were performed using R. was the only inhibitor overexpressed in breast tumors and showed significant associations with the Luminal B, HER2, TNBC, and normal-like subtypes, along with a modest increase across stages. , , and were downregulated in tumors. High expression of and correlated with better overall survival. -associated genes were enriched in NF-kappa and PI3K-Akt signaling and actin cytoskeleton components. was linked to Hedgehog and MAPK pathways and actin-related elements. correlated with Hedgehog and PI3K-Akt signaling, DNA damage response, and membrane components. TIMP4 was associated with VEGF, MAPK, PI3K-Akt, DNA damage pathways, and actin organization. showed strong positive correlations with and , while showed negative correlations with and . Interestingly, we found a strong positive correlation between and with , as well as between and with , and negative correlations with . The differential expression of TIMPs favors greater infiltration of immune cells related to tumor progression and poor prognosis in breast cancer patients. TIMPs display contrasting expression profiles and distinct pathway associations in breast cancer. emerges as the only consistently overexpressed inhibitor, while appears as a promising prognostic marker with unique MMP correlations that may influence tumor behaviors. - Source: PubMed
Publication date: 2026/02/02
Cayetano-Salazar LorenaGarcía-López Jhactcidi JackelineNava-Tapia Dania AHernández-López EymardWeinstein-Oppenheimer CarolineOrtiz-Ortiz JulioLeyva-Vázquez Marco AntonioMendoza-Catalán Miguel ÁngelArizmendi-Izazaga AdánNavarro-Tito Napoleón - A Disintegrin and metalloprotease (ADAM) family encompasses a diverse array of widely expressed proteases functioning in pathological processes. ADAM15 stands out as a pivotal mediator in multiple tumor types, responding to immune checkpoint inhibitors (ICI) significantly. By promoting pro-angiogenic genes, potentiating integrin binding as well as modulating the inflammatory response, ADAM15 orchestrates cellular adhesion and migration, thereby fostering tumor progression. Despite these compelling insights, the intricate roles of ADAM15 in prediction, immune modulation, and therapeutic targeting among malignant disorders remain largely unexplored. To decipher the pan-cancer landscape of ADAM15, we integrated data from multiple databases. Immunohistochemical profiles of ADAM15 were retrieved from the human protein atlas (HPA) database. Furthermore, the tumor immune estimation resource (TIMER) and the ESTIMATE (Estimation of Stromal and Immune cells in Malignant Tumor tissues using Expression data) algorithm were harnessed to dissect the immune infiltration patterns and immune checkpoint genes associated with ADAM15. The tumor immune single-sample gene set enrichment analysis (TISMO) was employed to explore the impact of ADAM15 on the tumor immune microenvironment. Additionally, drug sensitivity analysis and subsequent molecular docking studies were conducted to identify potential therapeutic compounds targeting ADAM15. These findings were rigorously validated through reverse transcription-polymerase chain reaction (RT-PCR), western blotting (WB), and immunohistochemistry (IHC) by cell lines and clinical samples from hepatocellular carcinoma (HCC) as well as colon adenocarcinoma (COAD). Our comprehensive analysis revealed that ADAM15 is markedly upregulated in diverse cancer types. IHC, WB, and RT-PCR assays of HCC and COAD confirmed these findings. Notably, elevated ADAM15 correlates with adverse prognosis in pan-cancer, positioning it as a promising novel biomarker. Drug sensitivity profiling unveiled a positive and statistically significant association between ADAM15 and AZD-8055 and Nitazoxanide, whereas a negative correlation was observed with Oxaliplatin and Ponatinib. These findings were further corroborated by molecular docking simulations, highlighting the potential of these compounds as therapeutic targets for ADAM15-driven cancers. Our study underscores the multifaceted role of ADAM15 in cancer progression, immune evasion, and response to therapy. By elucidating the intricate interplay between ADAM15 and the tumor microenvironment (TME), we have identified novel diagnostic biomarkers and potential therapeutic avenues. - Source: PubMed
Guo WenjiaLiu Yu'eMa WencongFan LieyingChen BingdiWang Jinghan - Idiopathic pulmonary fibrosis (IPF) is associated with poor prognosis. - Source: PubMed
Publication date: 2026/01/06
Yang WangPan Peng