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

Abstract

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 enzyme-linked 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.