Background: Cervical cancer is the leading cause of cancer-related mortality among females worldwide. Although previous studies have implicated tripartite motif-containing protein 37 (TRIM37) in the progression of various malignancies, its precise role and the underlying molecular mechanisms in cervical cancer remain inadequately explored.

Methods: TRIM37 expression, both at protein and mRNA levels, was assessed in immortalized keratinocytes and cervical cancer cell lines using RT-qPCR and Western blotting, respectively. The cervical cancer cells were transfected with TRIM37-specific siRNA employing Lipofectamine. Cellular proliferation, migration, and invasion were evaluated using Transwell assays, flow cytometry, colony formation assays, and cell counting kit (CCK)-8. Western blotting analysis was used to assess the phosphorylation status of proteins involved in the Phosphatase and Tensin Homolog Deleted on Chromosome Ten (PTEN)/Phosphatidylinositol-3-Kinase (PI3K)/Protein Kinase B (Akt)/Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. Interaction between TRIM37 and PTEN was examined via co-immunoprecipitation assays. Furthermore, an in vivo nude mice xenograft model was successfully established to assess the impact of TRIM37 on tumor growth.

Results: TRIM37 was substantially upregulated in cervical cancer cell lines compared to immortalized keratinocytes (p < 0.05). TRIM37 knockdown significantly suppressed proliferation, migration, and invasion in cervical cancer cells, thereby promoting apoptosis (p < 0.05). In vivo analysis revealed that TRIM37 knockdown significantly inhibited the growth of tumor (p < 0.05). Moreover, TRIM37 silencing effectively suppressed the activity of the PTEN/PI3K/Akt/NF-κB pathway in cervical cancer cells (p < 0.05).

Conclusions: TRIM37 knockdown inhibits cell proliferation, migration, and invasion, as well as suppresses in vivo tumor growth, potentially through downregulation of the PTEN/PI3K/Akt/NF-κB signaling pathway.