ArticleBiochemical genetics2025
TRIM8 Promotes Proliferation, Invasion, and Migration of Cervical Cancer Cells by Ubiquitinating and Degrading SOCS1.
Article in Biochemical genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- The application value of serum Th1/Th2 cytokines combined with tumour markers in the diagnosis of HR-HPV-positive cervical cancer.Journal of medical biochemistry · 2026Article
- The dynamic role of TRIM8, a novel ciliary protein, during various stages of mitosis.Cell death & disease · 2025Article
- Multifaceted role ofMedComm · 2024Review
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cervical cancer (CC) is a malignant tumor primarily caused by the persistent infection with high-risk strains of human papillomavirus. This study investigates the aberrant expression of Tripartite Motif Containing 8 (TRIM8) in CC and its impact on cell proliferation, invasion, and migration. Expression levels of TRIM8, Proliferating Cell Nuclear Antigen, and Suppressor of Cytokine Signaling 1 (SOCS1) were assessed in CC cell lines. CC cells were transfected with si-TRIM8, followed by cell counting kit-8 (CCK-8) assay, colony formation assay, and Transwell assay. Protein immunoprecipitation assay was employed to examine TRIM8's binding with SOCS1, and the ubiquitination level of SOCS1 was determined after MG132 treatment. Rescue experiments were conducted using si-SOCS1 and si-TRIM8 in combination. Results indicate upregulation of TRIM8 in CC cells. Inhibition of TRIM8 suppressed cell viability, proliferation, invasion, and migration. TRIM8 promoted CC cell proliferation, invasion, and migration of CC cells through ubiquitination-mediated degradation of SOCS1. Inhibition of SOCS1 partially reversed the inhibitory effects of si-TRIM8 on the proliferation, invasion, and migration of CC cells. In conclusion, TRIM8 enhances CC cell proliferation, invasion, and migration via ubiquitination-mediated degradation of SOCS1.
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Registered trials
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