Abstract

ObjectiveThis study investigated the role and mechanism of dual-specificity phosphatase 14 in cervical cancer.MethodsIn this experimental study, clinical samples from five patients with cervical squamous cell carcinoma and five with chronic cervicitis were analyzed. Dual-specificity phosphatase 14 was overexpressed in HeLa and SiHa cells. Gene and protein expression levels were analyzed using real-time quantitative polymerase chain reaction and western blot analysis. Cell viability, apoptosis, and migration were assessed using cell counting kit-8, flow cytometry as well as Transwell and wound healing assays. Cytokine levels were measured using enzyme-linked immunosorbent assay.ResultsDual-specificity phosphatase 14 expression was significantly downregulated in cervical cancer tissues and cell lines compared with that in their respective controls (p < 0.05). Dual-specificity phosphatase 14 overexpression markedly inhibited cell viability and induced apoptosis in HeLa and SiHa cells (p < 0.05). Furthermore, it significantly suppressed cell migration (p < 0.05). At the molecular level, dual-specificity phosphatase 14 upregulation decreased messenger ribonucleic acid levels of transforming growth factor-beta-activated kinase 1, NOD-like receptor pyrin domain containing 3, interleukin-1 beta, and tumor necrosis factor-alpha; reduced protein levels of phosphorylated transforming growth factor-beta-activated kinase 1 and NOD-like receptor pyrin domain containing 3; and diminished secretion of interleukin-1 beta and tumor necrosis factor-alpha cytokines (p < 0.05).ConclusionDual-specificity phosphatase 14 acts as a tumor suppressor in cervical cancer by inhibiting proliferation and migration, promoting apoptosis, and suppressing the transforming growth factor-beta-activated kinase 1/NOD-like receptor pyrin domain containing 3 inflammatory pathway, highlighting its potential as a novel therapeutic target and biomarker.