ArticleMolecular biotechnology2024
Comprehensive Analysis of ADAMTS Gene Family in Renal Clear Cell Carcinoma and ADAMTS10 Research Combining Magnetic Resonance Imaging.
Article in Molecular biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- ADAMTS2: More than a procollagen N-proteinase.Genes & diseases · 2025Review
- Associations of SEMA7A, SEMA4D, ADAMTS10, and ADAM8 with KRAS, NRAS, BRAF, PIK3CA, and AKT Gene Mutations, Microsatellite Instability Status, and Cytokine Expression in Colorectal Cancer Tissue.Current issues in molecular biology · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Clear cell renal carcinoma (ccRCC) is one of the cancers that posed a severe threat to human life on a global scale. The ADAMTS family has been proven to be involved in a number of tumor types, although it is yet unknown how they relate to ccRCC. The mRNA expression matrix and other clinically relevant information of 607 ccRCC were sourced from TCGA database. The role of ADAMTS family genes in ccRCC was determined by differential gene expression analysis and gene set enrichment analysis (GSEA). Employing stage grading, gene mutation, and survival analysis, the genes most linked to the prognosis of ccRCC were identified. The influence of genes on the pathway was determined by Kyoto Encyclopedia of Genes and Genes (KEGG) analysis. Following that, the gene's impact on ccRCC was verified by qRT-PCR, WB, MTT, Transwell detection, and a wound healing assay. Bioinformatics analysis showed that ADAMTS10 was overexpressed in cancerous tissues of people with ccRCC and its expression increased with tumor grade. Mutation analysis showed that the main cause of mutation in the ADAMTS family gene was amplification. The prognosis and survival of the ADAMTS10 elevated expression group were lower than those of the poorly expressed group, as demonstrated by a survival analysis. On the basis of the findings of MRI, we examined 60 clinical patients and collected their cancer along with the surrounding tissues. The results of qPCR detection showed that the expression of ADAMTS10 was considerably higher in cancerous regions of 60 clinical users than it was in the tissues nearby. Inhibiting ADAMTS10 development prevents cancer cells from proliferating, invading, and migrating. The KEGG analysis links ADAMTS10 to the NF-κB signal pathway. WB experiment confirmed that inhibiting ADAMTS10 expression can inhibit the activation of the NF-κB signal pathway. ADAMTS10 may be a promising prognostic marker for ccRCC that can be employed independently.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.