ArticleInternational journal of molecular sciences2025
Inhibitory Effect and Mechanism of the Down-Regulation of TRIM32 in Colorectal Cancer.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- TRIM32 drives head and neck squamous cell carcinoma progression via TP53 suppression and lysosomal/autophagy dysregulation.Translational cancer research · 2026Article
- A Swedish Haplotype GWAS in Familial and Sporadic Site-Specific Colorectal Cancer.International journal of molecular sciences · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
TRIM32 protein represents a crucial member of TRIM family that is highly expressed in numerous human cancers, and is associated with a poor prognosis. However, the mechanism of TRIM32 in colorectal cancer (CRC) is unclear. The expression of TRIM32 and its prognostic value in CRC were analyzed using The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database. Real-time quantitative PCR, immunohistochemistry (IHC), and cell proliferation assays were used to explore the effects of down-regulation of TRIM32 expression on the proliferation, migration, and apoptosis of cultured CRC cells (HCT116 and SW480 cells) and in xenogeneic tumorigenic animals. Bioinformatics analysis showed that TRIM32 is up-regulated in many types of cancers, and exhibits significant prognostic value in CRC. Western blotting results showed that after knocking down TRIM32, the expression level of IκBα increased, and the expression levels of TRIM32, p-p65, Bcl-2, and IKKβ decreased. The inhibitory effect of TRIM32 on CRC in vivo was evaluated by measuring tumor volume and weight, Hematoxylin and eosin (H&E) staining, and Ki67 IHC staining in heterotopic tumor-forming mice with CRC. Down-regulation of TRIM32 can inhibit the activation of the NF-κB signaling pathway and the occurrence of CRC. Our research provides a new insight into the pathogenesis of CRC, and a therapeutic target for the treatment of CRC.
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Registered trials
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