Knockout of promotes the migration and invasion of cervical cancer cells.

Background: Serine threonine kinase 10 () is an ERM kinase involved in the activation of ERM proteins and plays an essential role in the aggregation and adhesion of lymphocytes. STK10 is expressed in about 17 cancer types, including cervical cancer. Cervical cancer is the fourth most common cancer that seriously threatens women's health worldwide. Previous studies have shown that STK10 may affect LFA-1-mediated cell adhesion. Other studies reported a mutation (R634H) of detected in peripheral T-cell lymphoma. This study aimed to evaluate the functional roles of in the pathogenesis of cervical cancer.

Methods: We generated knockout cervical cancer cell lines using the CRISPR-Cas9 gene-editing system, and further analyzed the effects of STK10 deficiency on tumor biological behaviors. The proliferation, apoptosis, migration and invasive activity of these cells were respectively detected by BrdU incorporation, AnnexinV/propidium iodide (PI) staining, wound healing assay and Transwell assays without and with Matrigel. The phosphorylation and expression level of indicated proteins were analyzed by Western blot. The differential expression genes between knockout and control cells were identified by RNA-seq analysis and further confirmed using qRT-PCR.

Results: Our data revealed that target deletion of does not affect cell proliferation and apoptosis, but promotes the adhesion, migration, and invasion of cervical cancer cells. Most strikingly, the phosphorylation and expression level of ezrin and other ERM proteins in knockout cells was comparable with that in the control cells. Further, RNA-seq analysis indicated that the knockout of resulted in a profound alteration of gene expression in cervical cancer cells.

Conclusions: This is the first study to provide evidence that executes various physiological functions in addition to phosphorylation of ERM proteins, and plays a vital role in the migration and invasion of cervical cancer cells.