KLF14 targets ITGB1 to inhibit the progression of cervical cancer via the PI3K/AKT signalling pathway

Abstract

Abstract Our study aimed to determine whether Krüppel-like factor 14 (KLF14) inhibits the proliferation and promotes the apoptosis of cervical cancer cells through integrin β1 (ITGB1). Immunohistochemistry was performed to determine the expression of KLF14. The effect of KLF14 on the proliferation of cervical cancer cells was verified by Cell Counting Kit-8 (CCK-8) assays, colony formation assays and in vivo experiments. The effect of KLF14 on cervical cancer cell apoptosis was detected by flow cytometry. The targeting relationship between KLF14 and ITGB1 was evaluated by Western blotting and a dual-luciferase reporter assay. Moreover, Flow cytometry was performed to verify the relationship between KLF14 and ITGB1 on the apoptosis of cervical cancer cells. Additionally, Western blot analysis was performed to investigate the relationship between KLF14 and ITGB1 on the expression of downstream related molecules. As a result, the expression of KLF14 in cervical cancer tissues was lower than that in paracancerous tissues. KLF14 inhibited proliferation and promoted apoptosis in cervical cancer cells. Mechanistically, ITGB1 expression was significantly downregulated in KLF14-overexpressing cervical cancer cells. At the same time, we found that the effects of KLF14 and ITGB1 on apoptosis of cervical cancer cells could be mutually affected. KLF14 directly targeted ITGB1 to regulate its downstream PI3K/AKT signalling pathway. In summary, KLF14 inhibits the progression of cervical cancer by targeting ITGB1 via the PI3K/AKT signalling pathway.

Keywords

• Cervical cancer
• KLF14
• ITGB1
• PI3K/AKT signalling pathway
• Apoptosis