98%
921
2 minutes
20
Adhesion-regulating molecule 1 (ADRM1) has been implicated in tumor development, yet its specific role in bladder cancer (BC) remains undefined. This study aimed to elucidate the function of ADRM1 in BC through a combination of bioinformatics analysis and immunohistochemical analysis (IHC). Utilizing R version 3.6.3 and relevant packages, we analyzed online database data. Validation was conducted through IHC data, approved by the Institutional Ethics Committee (Approval No. K20220830). In both paired and unpaired comparisons, ADRM1 expression was significantly elevated in BC tissues compared to adjacent tissues, as evidenced by the results of TCGA dataset and IHC data. Patients with high ADRM1 expression had statistically worse overall survival than those with low ADRM1 expression in TCGA dataset, GSE32548 dataset, GSE32894 dataset, and IHC data. Functional analysis unveiled enrichment in immune-related pathways, and a robust positive correlation emerged between ADRM1 expression and pivotal immune checkpoints, including CD274, PDCD1, and PDCD1LG2. In tumor microenvironment, samples with the high ADRM1 expression contained statistical higher proportion of CD8 + T cells and Macrophage infiltration. Meanwhile, these high ADRM1-expressing samples displayed elevated tumor mutation burden scores and stemness indices, implying potential benefits from immunotherapy. Patients with low ADRM1 expression were sensitive to cisplatin, docetaxel, vinblastine, mitomycin C, and methotrexate. According to the findings from bioinformatics and IHC analyses, ADRM1 demonstrates prognostic significance for BC patients and holds predictive potential for both immunotherapy and chemotherapy responses. This underscores its role as a biomarker and therapeutic target in BC.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10491834 | PMC |
http://dx.doi.org/10.1038/s41598-023-41992-8 | DOI Listing |
Cancer Manag Res
August 2025
Department of Physiology, School of Basic Medical Sciences, Key Laboratory of Functional and Clinical Translational Medicine, Fujian Province University, Xiamen Medical College, Xiamen, 361023, People's Republic of China.
Background: Oral tongue squamous cell carcinoma (OTSCC), the most prevalent oral malignancy, lacks effective treatments.
Objective: Evaluate Evodia lepta ( ) as a potential OTSCC therapeutic.
Methods: Cell viability (CCK-8) and protein expression (Western blot) were assessed in OTSCC (CAL27, TCA8113) and 3T3 cells after 24h treatment with or cisplatin.
Am J Transl Res
January 2025
Department of Orthopedics, The Second Affiliated Hospital of Soochow University Suzhou 215004, Jiangsu, China.
Objective: Adhesion regulating molecule-1 (ADRM1), a 26S proteasome adaptor protein, plays a crucial role in mediating the growth and differentiation of osteoclasts in osteoporosis (OP). However, its involvement in this osteoanabolic effect remains largely uninvestigated.
Methods: experiments, including both gain-of-function and loss-of-function approaches, were conducted in MC3T3-E1 and C3H10T1/2 cells.
J Hepatol
July 2025
Department of Surgery, Sir Y.K. Pao Centre for Cancer, The Chinese University of Hong Kong, Shatin, Hong Kong, China. Electronic address:
Background & Aims: The ubiquitin receptor ADRM1/Rpn13 governs the specificity of eukaryotic protein degradation. We first discovered a novel spliced variant of ADRM1 with a skipped exon 9, termed ADRM1-ΔEx9, in human hepatocellular carcinoma (HCC) by SMRT sequencing. The aim of this study was to elucidate this novel ubiquitin receptor's underlying biology and clinical implications in HCC.
View Article and Find Full Text PDFCell Death Dis
July 2024
Institute of Digestive Diseases, Xuzhou Medical University, Xuzhou, Jiangsu, China.
It has been shown that the formation of filopodia is a key step in tumor cell metastasis, but there is limited research regarding its mechanism. In this study, we demonstrated that fatty acid synthase (FASN) promoted filopodia formation in liver cancer cells by regulating fascin actin-bundling protein 1 (FSCN1), a marker protein for filopodia. Mechanistically, on the one hand, the accumulation of FASN is caused by the enhanced deubiquitination of FASN mediated by UCHL5 (ubiquitin c-terminal hydrolase L5).
View Article and Find Full Text PDFPLoS One
July 2024
Department of Oncology, Johns Hopkins University, Baltimore, Maryland, United States of America.
There is an urgent unmet need for more targeted and effective treatments for advanced epithelial ovarian cancer (EOC). The emergence of drug resistance is a particular challenge, but small molecule covalent inhibitors have promise for difficult targets and appear less prone to resistance. Michael acceptors are covalent inhibitors that form bonds with cysteines or other nucleophilic residues in the target protein.
View Article and Find Full Text PDF