ArticleOncoTargets and therapy2018
TRIM37 promotes cell invasion and metastasis by regulating SIP1-mediated epithelial-mesenchymal transition in gastric cancer.
Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Activation of TRIM37 by ATF6 and degradation of ACSL4: inhibiting ferroptosis and propelling cervical cancer progression.Hereditas · 2025Article
- Therapeutic potential of TRIM family proteins in gastric cancer: from signaling pathway regulation to precision targeting strategies.Frontiers in oncology · 2025Review
- Review
- Intricate confrontation: Research progress and application potential of TRIM family proteins in tumor immune escape.Journal of advanced research · 2023Review
- TRIM37 Promotes Pancreatic Cancer Progression through Modulation of Cell Growth, Migration, Invasion, and Tumor Immune Microenvironment.International journal of molecular sciences · 2022Article
- TRIM37 interacts with PTEN to promote the growth of human T-cell acute lymphocytic leukemia cells through regulating PI3K/AKT pathway.Frontiers in oncology · 2022Article
- TRIM37: a critical orchestrator of centrosome function.Cell cycle (Georgetown, Tex.) · 2021Review
- Circular RNA circRNA_101996 promoted cervical cancer development by regulating miR-1236-3p/TRIM37 axis.The Kaohsiung journal of medical sciences · 2021Article
- Roles of E3 ubiquitin ligases in gastric cancer carcinogenesis and their effects on cisplatin resistance.Journal of molecular medicine (Berlin, Germany) · 2021Review
- ASB16-AS1 up-regulated and phosphorylated TRIM37 to activate NF-κB pathway and promote proliferation, stemness, and cisplatin resistance of gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2021Article
- TRIM37 contributes to malignant outcomes and CDDP resistance in gastric cancer.Journal of Cancer · 2021Article
- ROS/NF-κB Signaling Pathway-Mediated Transcriptional Activation of TRIM37 Promotes HBV-Associated Hepatic Fibrosis.Molecular therapy. Nucleic acids · 2020Article
- Diosgenin and GSK126 Produce Synergistic Effects on Epithelial-Mesenchymal Transition in Gastric Cancer Cells by Mediating EZH2 via the Rho/ROCK Signaling Pathway.OncoTargets and therapy · 2020Article
- The Tripartite Nexus: Autophagy, Cancer, and Tripartite Motif-Containing Protein Family Members.Frontiers in pharmacology · 2020Review
- TRIM37 Mediates Chemoresistance and Maintenance of Stemness in Pancreatic Cancer CellsFrontiers in oncology · 2020Article
- Knockdown of TRIM37 Promotes Apoptosis and Suppresses Tumor Growth in Gastric Cancer by Inactivation of the ERK1/2 Pathway.OncoTargets and therapy · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTripartite motif containing 37 (TRIM37) has been demonstrated to function importantly during the progression of various cancers. However, the role of TRIM37 in gastric cancer (GC) remains elusive. MATERIALS AND
methodsTRIM37 mRNA and protein expressions were determined by qRT-PCR, Western blot, and immunohistochemical staining in GC specimens. The effects of TRIM37 on GC cells behavior were evaluated by transwell assays in vitro and metastasis assay in vivo, respectively. Besides, qRT-PCR, Western blot, and immunofluorescence staining were employed to detect the expressions of TRIM37 and epithelial-mesenchymal transition (EMT)-related markers.
resultsThe present study revealed that TRIM37 mRNA or protein expression was significantly increased in GC tissues compared with that in paracancerous control tissues, and its aberrant overexpression was closely associated with clinical metastasis and poor prognosis in patients with GC. TRIM37 knockdown significantly suppressed GC cells migration and invasion in vitro, as well as metastasis in vivo. Inversely, TRIM37 overexpression exerted the opposite effects. Mechanistic studies suggested that SIP1-mediated EMT might be responsible for TRIM37-facilitated GC cells migration and invasion.
conclusionOur findings revealed that high TRIM37 expression was associated with clinical metastasis and poor survival in patients with GC. TRIM37 promoted GC cells migration and invasion via EMT, mediated by the transcription factor SIP1, thus providing a candidate target for GC treatment.
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