KLF5-mediated Eppk1 expression promotes cell proliferation in cervical cancer via the p38 signaling pathway

Abstract Background Epiplakin1 (Eppk1) is part of epidermal growth factor (EGF) signal and takes in reorganization cytoskeleton cell proliferation. However, the role Eppk1 cervical cancer (CC) remains unknown. Methods To express KLF5 their correlation, we used RNA-sequence, RT-qPCR, TCGA database immunofluorescence staining vitro different pathological tissues. In CC lines, tested adenovirus-mediated over expression or knockdown siRNA-mediated a suiting assessment proliferation signaling by western blot CCK8 tests. We studied mechanism which regulates reporter gene test chromatin immunoprecipitation test. Results promoted tissues lines compared with increased expression. The results further showed co-expression correlated substantially tumorigenesis Overexpression significantly at transcription translation levels. Conversely, siRNA against decreased Mechanically, activated direct binding to promoter. Gain- loss-of-function experiments reported that Hela partly dependent on upregulation. Besides, KLF5-mediated activation p38 after decline proliferation, suggesting lies upstream affecting Finally, positively tumor size clinicopathological features CC. Conclusions may be an effective therapeutic target for pathway cancer.