TRIM27 Promotes the Progression of Laryngeal Cancer by Activating the IL-6/JAK-STAT Signaling Pathway

Backgrounds: Laryngeal cancer manifests as a malignant tumor, often leading to unfavorable prognosis for patients. There is a pressing need for potential biomarkers and therapeutic targets for laryngeal cancer. Our study delved into the role of tripartite motif-containing 27 (TRIM27) in laryngeal cancer cells and studied the effect of interleukin-6 (IL-6) coupled with janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway on the pathogenesis of laryngeal cancer.Methods: Initially, using the quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), we investigated the expression levels of TRIM27 in both normal epithelial cells (NP69) and laryngeal cancer cells (Hep2). Subsequently, the effects of TRIM27 on IL-6 inflammatory factors and JAK-STAT pathway-associated proteins were measured using enzymelinked immunosorbent assay (ELISA) and western blot, respectively. Finally, the mechanism of TRIM27 on the growth and metastasis of Hep2 cells was assessed through cell counting kit 8 (CCK8), flow cytometry, and transwell assays.Results: Compared to the normal epithelial cell NP69, TRIM27 levels in the laryngeal cancer cell Hep2 were markedly increased (p < 0.001). TRIM27 overexpression has increased IL-6 levels, activated the JAK-STAT pathway, and increased p-JAK2 and p-STAT3 protein levels. Conversely, silencing TRIM27 inhibited the proliferation and metastasis of Hep2 cells by blocking the JAK-STAT pathway, especially when compared to overexpressing TRIM27 (OE-TRIM27) (p < 0.001).Conclusions: This study demonstrates that silencing TRIM27 can effectively inhibit the progression of laryngeal cancer cells through the deactivation of the IL-6/JAK-STAT pathway, indicating that TRIM27 may be a promising target for laryngeal cancer treatment.

Automated summary

This study investigated the role of TRIM27 in laryngeal cancer cells and the effects of IL-6 coupled with JAK-STAT signaling pathway on the pathogenesis of laryngeal cancer.