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BIOMARKER:

ADAM9 expression

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Other names: ADAM9, ADAM Metallopeptidase Domain 9, MCMP, MDC9, Disintegrin And Metalloproteinase Domain-Containing Protein 9, Metalloprotease/Disintegrin/Cysteine-Rich Protein 9, Cellular Disintegrin-Related Protein, Myeloma Cell Metalloproteinase, Cone Rod Dystrophy 9, Mltng, A Disintegrin And Metalloproteinase Domain 9 (Meltrin Gamma), ADAM Metallopeptidase Domain 9 (Meltrin Gamma), Meltrin-Gamma, CORD9
Entrez ID:
Related biomarkers:
4ms
Exosomal circ_0000735 contributes to non-small lung cancer malignant progression. (PubMed, J Biochem Mol Toxicol)
In addition, exosomes mediated the intercellular transmission of circ_0000735, and serum exosomal circ_0000735 might be an important indicator for the diagnosis of NSCLC. In conclusion, circ_0000735 facilitated NSCLC progression via miR-345-5p/ADAM19 pathway, and serum exosomal circ_0000735 might be a potential biomarker for NSCLC diagnosis.
Journal
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ADAM9 (ADAM Metallopeptidase Domain 9) • MIR345 (MicroRNA 345)
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ADAM9 expression • ADAM9 overexpression
4ms
Exploring the oncogenic and tumor-suppressive roles of Circ-ADAM9 in cancer. (PubMed, Pathol Res Pract)
Additionally, the review explores the possibility of Circ-ADAM9 as a valuable biomarker, offering insights into its prognostic, diagnostic, and therapeutic implications. By summarizing the latest discoveries in this field, the review contributes to our understanding of the multifaceted contribution of Circ-ADAM9 in tumor biology and its potential applications in clinical settings.
Review • Journal
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ADAM9 (ADAM Metallopeptidase Domain 9)
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ADAM9 expression
5ms
YY1-induced lncRNA00511 promotes melanoma progression via the miR-150-5p/ADAM19 axis. (PubMed, Am J Cancer Res)
Rescue assays indicated that LINC00511 acted as a competing endogenous RNA (ceRNA) to sponge miR-150-5p and increase the expression of ADAM19, thereby activating the PI3K/AKT pathway. In summary, we identified LINC00511 as an oncogenic lncRNA in melanoma and defined the LINC00511/miR-150-5p/ADAM19 axis, which might be considered a potential therapeutic target and novel molecular mechanism the treatment of patients with melanoma.
Journal
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ADAM9 (ADAM Metallopeptidase Domain 9) • MIR150 (MicroRNA 150) • YY1 (YY1 Transcription Factor)
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ADAM9 expression
5ms
Therapeutic restoration of miR-126-3p as a multi-targeted strategy to modulate the liver tumor microenvironment. (PubMed, Hepatol Commun)
A directed RNA therapeutic approach can mitigate NK cell immune evasion, reduce angiogenesis, and alter the tumor cell phenotype through the restoration of miR-126-3p in liver tumor cells. The pleiotropic effects elicited by this multi-targeted approach to modulate the local tumor microenvironment support its use for the treatment of liver cancer.
Journal
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ADAM9 (ADAM Metallopeptidase Domain 9) • MIR126 (MicroRNA 126)
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ADAM9 expression
7ms
Long non-coding RNA LINC00565 regulates ADAM19 expression through sponging microRNA-532-3p, thereby facilitating clear cell renal cell carcinoma progression. (PubMed, Chin J Physiol)
Overexpressed ADAM19 could eliminate the anticancer effects caused by knocking down LINC00565 on ccRCC cells. In conclusion, LINC00565 upregulated ADAM19 via absorbing miR-532-3p, thereby facilitating the progression of ccRCC cells.
Journal
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ADAM9 (ADAM Metallopeptidase Domain 9) • AGO2 (Argonaute RISC Catalytic Component 2) • MIR532 (MicroRNA 532)
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ADAM9 expression • ADAM9 overexpression
8ms
Circ_0061140 Potentiates Clear Cell Renal Cell Carcinoma Progression Via the MicroRNA-126-5p/ADAM9 Axis. (PubMed, Mol Biotechnol)
It was suggested that suppressed miR-126-5p or overexpressed ADAM9 induced cell proliferation and restricted cell apoptosis in ccRCC cells based on si-circ_0061140 (p < 0.01). Altogether, this study highlights that circ_0061140 plays an oncogenic role in ccRCC through modulation of the miR-126-5p/ADAM9 axis.
Journal
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ADAM9 (ADAM Metallopeptidase Domain 9) • MIR126 (MicroRNA 126)
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ADAM9 expression • ADAM9 overexpression • miR-126-3p overexpression
8ms
Licochalcone A Inhibits Proliferation and Metastasis of Colon Cancer by Regulating miR-1270/ADAM9/Akt/NF-κB axis. (PubMed, Iran J Public Health)
LCA and miR-1270 mimic inactivated the Akt/NF-κB pathway, while ADAM9 over-expression rescued it. LCA exhibited antitumor efficacy in HCT116 cells by inhibiting the Akt/NF-κB signaling pathway by regulating the miR-1270/ADAM9 axis.
Journal
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ADAM9 (ADAM Metallopeptidase Domain 9) • MIR127 (MicroRNA 127)
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ADAM9 expression • ADAM9 overexpression
1year
Functional characteristics of DNA N6-methyladenine modification based on long-read sequencing in pancreatic cancer. (PubMed, Brief Funct Genomics)
In addition, the distinction for pancreatic cancer subtypes was determined using 46 subtype-specific genes and unsupervised clustering. Overall, our study is the first to explore the molecular characteristics of 6mA modifications in pancreatic cancer, indicating that 6mA has the potential to be a target for future clinical treatment.
Journal
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ADAM9 (ADAM Metallopeptidase Domain 9) • ADAM10 (ADAM Metallopeptidase Domain 10) • LAMA3 (Laminin Subunit Alpha 3)
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ADAM9 expression
over1year
The ADAM9/WISP-1 axis cooperates with osteoblasts to stimulate primary prostate tumor growth and metastasis. (PubMed, Int J Biol Sci)
Our study suggests that the ADAM9/WISP-1 axis assists with metastatic PCa progression. Thus, targeting the ADAM9/WISP-1 axis may help to prevent the malignant phenotypes of PCa cells.
Journal
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CDH1 (Cadherin 1) • ADAM9 (ADAM Metallopeptidase Domain 9) • CDH2 (Cadherin 2)
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ADAM9 expression • CDH1 expression
over1year
Extracellular vesicle‑mediated miR‑126‑3p transfer contributes to inter‑cellular communication in the liver tumor microenvironment. (PubMed, Int J Oncol)
Manipulation of miR‑126‑3p either by enforced expression using pre‑miR‑126‑3p or by inhibition using antimiR‑126‑3p did not alter tumor cell viability, proliferation or sensitivity to either sorafenib or regorafenib. Within LC/HSC spheroids, ADAM9 and vascular endothelial growth factor expression was increased by silencing of miR‑126‑3p but diminished with the restoration of miR‑126‑3p. These studies implicate miR‑126‑3p in functional effects on migration, invasion and spheroid growth of tumor cells in the presence of HSCs, and thereby demonstrate functional EV‑RNA‑based intercellular signaling between HSCs and LC cells that is directly relevant to tumor‑cell behavior.
Journal
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ADAM9 (ADAM Metallopeptidase Domain 9) • MIR126 (MicroRNA 126)
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ADAM9 expression • VEGFA expression
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sorafenib • Stivarga (regorafenib)
over1year
The role of ADAM9 in the tumor microenvironment and as a potential target for cancer vaccine (LCC 2023)
We found that recombinant ADAM9 could completely inhibit tumor growth. These results indicated that ADAM9 is important in tumor progressing and could be a good candidate for cancer vaccine.
CD8 (cluster of differentiation 8) • IFNG (Interferon, gamma) • ADAM9 (ADAM Metallopeptidase Domain 9)
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ADAM9 expression
over1year
Unfavorable immunotherapy plus tyrosine kinase inhibition outcome of metastatic renal cell carcinoma after radical nephrectomy with increased ADAM9 expression. (PubMed, Immunogenetics)
Expression of ADAM9 was also associated with the exhaustion and dysfunction of T cells. ADAM9-based RFscore has the potential to be used as a biomarker to distinguish the optimal patient treatment methods between IO-TKI and TKI monotherapy.
Journal • IO biomarker
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CD8 (cluster of differentiation 8) • ADAM9 (ADAM Metallopeptidase Domain 9) • CD4 (CD4 Molecule) • GZMB (Granzyme B)
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ADAM9 expression
almost2years
Journal
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ADAM9 (ADAM Metallopeptidase Domain 9) • MIR383 (MicroRNA 383)
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ADAM9 expression • ADAM9 overexpression
almost2years
Metalloprotease ADAM9 cleaves ephrin-B ligands and differentially regulates Wnt and mTOR signaling downstream of Akt kinase in colorectal cancer cells. (PubMed, J Biol Chem)
Surprisingly, we also found that KD of ADAM9 downregulates Wnt signaling, but has negligible effects on mTOR signaling in SW620 cells; in contrast, mTOR activity is suppressed while Wnt signaling remains unaffected by ADAM9 KD in HCT116 cells. These results suggest that mammalian ADAM9 cleaves ephrin-Bs to derepress Akt and promote CRC migration and invasion; however, the signaling pathways downstream of Akt are differentially regulated by ADAM9 in different CRC cell lines, reflecting the heterogeneity of CRC cells in responding to manipulations of upstream Akt regulators.
Journal
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ADAM9 (ADAM Metallopeptidase Domain 9)
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ADAM9 expression
almost2years
Exosomal circPABPC1 promotes colorectal cancer liver metastases by regulating HMGA2 in the nucleus and BMP4/ADAM19 in the cytoplasm. (PubMed, Cell Death Discov)
Our findings indicated that exosomal circPABPC1 is an essential regulator in CRC liver metastasis progression by promoting HMGA2 and BMP4/ADAM19 expression. CircPABPC1 is expected to be a novel biomarker and antimetastatic therapeutic target in CRC.
Journal
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ADAM9 (ADAM Metallopeptidase Domain 9) • HMGA2 (High mobility group AT-hook 2)
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ADAM9 expression
2years
Preclinical Evaluation of IMGC936, a Next Generation Maytansinoid-based Antibody-drug Conjugate Targeting ADAM9-expressing Tumors. (PubMed, Mol Cancer Ther)
Our preclinical data provide a strong scientific rationale for the further development of IMGC936 as a therapeutic candidate for the treatment of ADAM9-positive cancers. A first-in-human study of IMGC936 in patients with advanced solid tumors has been initiated (NCT04622774).
Preclinical • Journal
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ADAM9 (ADAM Metallopeptidase Domain 9)
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ADAM9 expression
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izeltabart tapatansine (IMGC936)
2years
Relevance of A Disintegrin and Metalloproteinase Domain-Containing (ADAM)9 Protein Expression to Bladder Cancer Malignancy. (PubMed, Biomolecules)
Moreover, in the gene expression omnibus (GEO) study, bladder cancer with surrounding carcinoma and invasive carcinoma showed significantly high ADAM9 mRNA expression. We found that ADAM9 knockdown suppressed cell proliferation and migration in bladder cancer and that high-grade bladder cancer is correlated with higher expression of ADAM9.
Journal
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ADAM9 (ADAM Metallopeptidase Domain 9)
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ADAM9 expression