Abstract
Cervical cancer is one of the most common gynecological malignancies worldwide. However, the pathogenesis of cervical cancer remains to be fully elucidated. Increasing evidence shows that microRNAs (miRNAs) may be involved in the pathogenesis of cervical cancer. The present study tested the hypothesis that the overexpression of miRNA (miR)‑411 may delay, whereas the overexpression of serine/threonine kinase 17a (STK17A) may contribute to, cervical cancer development and progression through the p53 pathway. Cervical cancer tissues and adjacent normal tissues were obtained from 141 patients with cervical cancer following radiotherapy, with efficacy evaluated. The receiver operating characteristic curve was plotted to show the value of miR‑411 and STK17A in predicting the efficacy of radiotherapy. Cox's proportional hazards regression model was utilized for multivariate analysis. A series of inhibitors, mimics or small interfering RNAs against STK17A were introduced to validate the regulatory mechanism of miR‑411 in governing STK17A, determined with a luciferase reporter gene assay. The expression of miR‑411 and STK17A, and the status of the p53 signaling pathway were evaluated. The colony forming ability, proliferation, migration, invasion and apoptosis of CaSki cells were assessed using a colony formation assay, 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide assay, Transwell assay and flow cytometry, respectively. miR‑411 was upregulated but STK17A was reciprocal in cervical tissues. The overexpression of miR‑411 and low expression of STK17A were correlated with high efficacy of radiotherapy. miR‑411 and STK17A had predictive value for the efficacy of radiotherapy; miR‑411 was the protective factor and STK17A was a risk factor for prognosis of cervical cancer. Increasing miR‑411 activated the p53 signaling pathway and promoted cell apoptosis, but inhibited cell proliferation, invasion and migration. STK17A, an miR‑411 target, increased following miR‑411 over‑expression, whereas the p53 signaling pathway was activated following STK17A inhibition. It was observed that the effect of miR‑411 inhibition was lost following STK17A silencing. These findings indicate that the miR‑411‑mediated direct suppression of STK17A induces apoptosis and suppresses the proliferation, migration and invasion of human cervical cancer cells via the p53 signaling pathway. Additionally, miR‑411 and STK17A have predictive value for the efficacy of radiotherapy.