ArticleTechnology in cancer research & treatment
TRIM11 Posttranscriptionally Modulated by miR-5193 Facilitates Tumor Growth and Metastasis of Prostate Cancer.
Article in Technology in cancer research & treatment. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- TRIM11 is upregulated in esophageal cancer and promotes tumor progression through modulation of the β-catenin signaling pathway.Functional & integrative genomics · 2026Article
- Review
- Targeting EGFR-TKI resistance in lung cancer: Role of miR-5193/miR-149-5p loaded NK-EVs and Carboplatin combination.International journal of pharmaceutics · 2025Article
- The impact of dysregulation SUMOylation on prostate cancer.Journal of translational medicine · 2025Review
- Article
- Multifaceted role ofMedComm · 2024Review
- TRIM11 Prevents Ferroptosis in model of asthma by UBE2N-TAX1BP1 signaling.BMC pulmonary medicine · 2024Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTripartite motif-containing protein 11 (TRIM11), an E3 ubiquitin ligase, possesses a pro-tumor property. Still, the detailed functions of TRIM11 remain not well characterized in prostate cancer.
methodsPC-3 and DU145 prostate cancer cells were transfected with small interfering RNAs (siRNAs) or lentiviruses for TRIM11 deficiency or overexpression, and microRNA-5193 (miR-5193) mimics were utilized for overexpressing miR-5193. Proliferation, apoptosis, migration, and invasion were examined through CCK-8, colony formation, flow cytometry, wound healing, and transwell assays. MAP kinase-extracellular signal-regulated kinase (MEK1/2) and extracellular signal-regulated kinase (ERK)1/2 activities were detected via immunoblotting. Murine xenograft models were established. Interactions of TRIM11 with miR-5193 were demonstrated via dual luciferase reporter.
resultsTRIM11 deficiency or miR-5193 overexpression exerted antiprostate cancer effects through suppression of proliferation, migration, and invasion as well as enhancement of apoptosis in PC-3 and DU145 cells. The mechanisms by which TRIM11 deficiency or miR-5193 overexpression involved the inactivation of MEK1/2 and ERK1/2. miR-5193 downregulated TRIM11 expressions in prostate cancer cells, and their interactions were confirmed. Further, up-regulated miR-5193 weakened the effects of TRIM11 overexpression on enhancing proliferation, migration, invasion, and activity of MEK1/2 and ERK1/2 as well as alleviating apoptosis of prostate cancer cells. In murine xenograft models, TRIM11 upregulation facilitated tumor growth, which was alleviated by miR-5193 overexpression.
conclusionThese findings described the oncogenic role of TRIM11 in prostate cancer biology, which was post-transcriptionally modulated by miR-5193.
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