Abnormal expression of long non-coding RNAs (lncRNAs) has been demonstrated to be a vital regulatory factor in a large number of malignancies. The investigation in cervical cancer and the associated modulation mechanisms are yet to be probed. The aim of this study is to specifically investigate the expression pattern and modulatory mechanism of MIR205HG in cervical cancer. Our paper firstly revealed the up-regulation of KRT17 in cervical cancer. Function assays further displayed that KRT17 silencing impaired the proliferation and migration, and activated the apoptosis of cervical cancer cells. Based on the finding that MIR205HG could regulate KRT17 expression, we further probed the detailed mechanism between MIR205HG and KRT17. It was observed from mechanism experiments that MIR205HG depleted SRSF1 to increase KRT17 expression. The whole mechanism of MIR205HG/SRSF1/KRT17 axis affecting cell proliferation, apoptosis and migration in cervical cancer was validated using rescue assays. In conclusion, MIR205HG modulated the biological activities of cervical cancer cells via targeting SRSF1 and regulating KRT17, which better understood the pathogenesis of cervical carcinoma and excavated a novel therapeutic target.