Williams syndrome transcription factor promotes proliferation and invasion of cervical cancer cells by regulating PI3K/Akt signaling pathway

Objective This study aimed to investigate the expression of Williams Syndrome transcription factor (WSTF) in cervical cancer (CC) tissues and cells, the effect on the proliferation, migration, invasion, and the molecular mechanism of WSTF in CC cells to find a new biomarker. Materials and Methods The expression of WSTF in tissues was detected by real-time quantitative polymerase chain reaction (RT-qPCR) and/or immunohistochemistry. Human CC cell lines and human normal cervical epithelial cell lines were detected by RT-qPCR. Lentivirus-mediated gene transfected in Siha/CaSki cells. The transfection efficiency of lentivirus was observed by a fluorescence microscope, RT-qPCR, and western blot. After transfection, the proliferation of Siha/CaSki cells was detected by CCK-8 assay and colony formation assay. The migration and invasion of Siha/CaSki cells were detected by transwell assay and wound healing assay. Western blot assay were used to detect the expression of WSTF and PI3K/Akt-related proteins in Siha/CaSki cells. Results The expression of WSTF in CC tissues was higher than that in adjacent tissues (p < 0.05). The expression of WSTF in CC cells was higher than that in normal cervical epithelial cells (p < 0.01). Downregulation of WSTF expression could inhibit the proliferation, migration, and invasion of CC cells (p < 0.01). WSTF overexpression activates PI3K/Akt signaling pathway (p < 0.01). Conclusion WSTF is highly expressed in CC tissues and cells, and downregulation of WSTF can inhibit the proliferation, invasion, and migration of CC cells by activating the PI3K/Akt signaling pathway. WSTF is a very promising new biomarker for CC.