ArticleJournal of translational medicine2026
Induction of TRIM22 promotes autophagy and apoptosis of colorectal cancer through reactive oxygen species generation.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundColorectal cancer (CRC) is one of the most common causes of cancer-associated death worldwide, and a rapid increase in the incidence and mortality of CRC has been predicted with a marked trend in the younger age group. Therefore, identifying novel therapeutic targets and developing effective therapies for CRC treatment is needed. Tripartite motif 22 (TRIM22) has been implicated in several cancers; however, its role in CRC therapy remains unknown.
methods¹H NMR, ¹³C NMR, high-resolution mass, and high performance liquid chromatography were used to determine novel pyrroloquinoline-polyamine analogues. MTT and colony formation assays were employed to detect the effects of TRIM22 and a novel pyrroloquinoline-polyamine analogue 8d on CRC. Flow cytometry was used to detect apoptosis, reactive oxygen species (ROS), and lysosomal pH. Transmission electron microscope, mCherry-GFP-LC3 plasmid, and monodansylcadaverine were utilized to examine autophagy. Cellular thermal shift assay, surface plasmon resonance, and a comprehensive computational analysis were used to investigate the interaction between TRIM22 and compound 8d. Western blotting and qRT-PCR analysis were performed to examine changes in protein and mRNA levels. Animal models were established to investigate the role of TRIM22 and compound 8d in progression of CRC.
resultsIn this study, we found that TRIM22 inhibited tumor growth of CRC in vitro and in vivo, and identified a novel pyrroloquinoline-polyamine analogue, designated compound 8d, which upregulated the protein levels of TRIM22 in both CRC cells and tumor tissues. Compound 8d directly bound to TRIM22 and increased its stability. Compound 8d significantly suppressed tumor growth and pulmonary metastasis of CRC in vitro and in vivo. Genetic inhibition of TRIM22 reversed the inhibitory effects of compound 8d on CRC in vitro and in vivo. TRIM22 silencing decreased compound 8d-induced nuclear factor erythroid 2-related factor 2 downregulation and ROS-mediated autophagy and apoptosis.
conclusionThese findings highlighted the potential of compound 8d as a promising anticancer agent and targeting TRIM22 may provide a novel therapeutic approach for CRC treatment.
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