TRIM37 (Tripartite Motif Containing 37) is an E3 ubiquitin ligase for histone H2A and inhibits transcription in several genes. However, it is not known whether it plays a role in gastric cancer (GC). In this study, we tested whether TRIM37 acts as a cancer-promoting factor by being overexpressed in GC. We analyzed GC cell lines and 124 primary tumors, which were curatively resected in our hospital between 2001 and 2003. Overexpression of the TRIM37 protein was detected in almost all GC cell lines and GC samples (76 out of 124 cases) and was significantly correlated with lymphatic and venous invasion, advanced T-Stage, N-Stage, histology and high recurrence rate. Patients with TRIM37 overexpressing tumors had a worse survival rate than those with non-expressing tumors (=0.0057). Moreover, TRIM37 positivity was identified as an independent factor predicting worse outcomes (=0.018, Hazard ratio 3.41). The apoptotic cell analysis showed that the knockdown of TRIM37 increased apoptosis in comparison with the control. In TRIM37 overexpressing GC cells, knockdown of TRIM37 suppressed the migration and invasion. TRIM37 plays a crucial role in tumor malignant potential through its overexpression and highlight its usefulness as a prognostic factor and potential therapeutic target in GC.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7739001 | PMC |
| http://dx.doi.org/10.7150/jca.47577 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
TRIM37 exacerbates cerebral ischemic injury by regulating the PPARγ/NF-κB pathway.
Neuroreport
February 2025
Department of Neurosurgery, the First Affiliated Hospital of Hainan Medical University, Haikou.
Ischemic stroke is the primary cause of mortality for individuals with disability worldwide. Tripartite motif 37 (TRIM37) plays multiple regulatory roles in various cellular processes. Our research aimed to investigate the effects of TRIM37 on the progression of ischemic stroke and its related mechanisms.
View Article and Find Full Text PDFThe TRIM37 variant rs57141087 contributes to triple-negative breast cancer outcomes in Black women.
EMBO Rep
November 2024
Department of Medical Microbiology and Immunology, University of California Davis School of Medicine, Davis, CA, 95616, USA.
Triple-negative breast cancer (TNBC) disproportionately affects younger Black women, who show more aggressive phenotypes and poorer outcomes than women of other racial identities. While the impact of socioenvironmental inequities within and beyond health systems is well documented, the genetic influence in TNBC-associated racial disparities remains elusive. Here, we report that cancer-free breast tissue from Black women expresses TRIM37 at a significantly higher level relative to White women.
View Article and Find Full Text PDFSkeletal Phenotype in Mulibrey Nanism, A Monogenic Skeletal Dysplasia With Fibrous Dysplasia.
Clin Genet
November 2024
Children's Hospital, Pediatric Research Center, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Article Synopsis
- - Mulibrey nanism (MUL) is a genetic growth disorder linked to mutations in the TRIM37 gene, leading to growth failure, distinct facial features, heart issues, infertility, and higher cancer risk.
- - A study of 33 MUL patients, aged 4.5-48 years, assessed their long bones and spine through radiographs, revealing significant skeletal abnormalities such as slender and bowed long bones, thick cortices, and tall vertebral bodies.
- - The study confirmed that all patients had skeletal changes, with 58% showing fibrous dysplasia and 52% having a history of fractures, highlighting TRIM37's critical role in skeletal development and maintenance.
Mesoscale regulation of MTOCs by the E3 ligase TRIM37.
bioRxiv
October 2024
Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Centrosomes ensure accurate chromosome segregation during cell division. Although the regulation of centrosome number is well-established, less is known about the suppression of non-centrosomal MTOCs (ncMTOCs). The E3 ligase TRIM37, implicated in Mulibrey nanism and 17q23-amplified cancers, has emerged as a key regulator of both centrosomes and ncMTOCs.
View Article and Find Full Text PDFTRIM37 employs peptide motif recognition and substrate-dependent oligomerization to prevent ectopic spindle pole assembly.
bioRxiv
October 2024
Department of Cell & Developmental Biology, School of Biological Sciences, University of California San Diego, La Jolla, California 92093, USA.
Tightly controlled duplication of centrosomes, the major microtubule-organizing centers of animal cells, ensures bipolarity of the mitotic spindle and accurate chromosome segregation. The RBCC (RING-B-box-coiled coil) ubiquitin ligase TRIM37, whose loss is associated with elevated chromosome missegregation and the tumor-prone developmental human disorder Mulibrey nanism, prevents the formation of ectopic spindle poles that assemble around structured condensates containing the centrosomal protein centrobin. Here, we show that TRIM37's TRAF domain, unique in the extended TRIM family, engages peptide motifs in centrobin to suppress condensate formation.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!