Interference with XPO1 Suppresses the Stemness and Radioresistance of CD44 Positive Cervical Cancer Cells via Binding with Rad21

Objective Cancer stem cells (CSCs) are responsible for cervical cancer progression and decreased radiosensitivity of tumor cells. Thepresent work is meant to illuminate the impacts of exportin 1 (XPO1) on the aggressive behaviors and radiosensitivity of cervicalcancer stemness cells and make a deeper inquiry into its regulatory mechanism despite that XPO1 has been supported to elicitsignificant activities on multiple malignancies. Methods XPO1 and Rad21 expression in HeLa (CD44+) cells was tested by RT-qPCR and western blot. Cell viability was estimated via CCK-8 assay. Cell stemness was examined viasphere formation assay and western blot. Following radiation treatment, cell proliferation was judged by CCK-8 assay, westernblot as well as EdU staining whereas TUNEL assay, RT-qPCR and western blot analysis appraised cell apoptosis. Cell radiosensitivitywas assessed through clonogenic survival assay. The levels of DNA damage markers were tested by western blot and related kits.STRING database and Co-IP assay respectively predicted and testified the binding of XPO1 with Rad21. RT-qPCR and western blotalso examined the expression of XPO1 cargoes. Results The experimental data corroborated that XPO1 and Rad21 were overexpressed in cervical cancer tissues and cells. XPO1 inhibitorKPT-330 impeded the stemness while elevated the radiosensitivity of HeLa (CD44+) cells. XPO1 bond to Rad21 and positively modulated Rad21 expression. Moreover, Rad21 elevation reversed the impacts of KPT-330on the behaviors of cervical cancer stemness cells. Conclusion To sum up, XPO1 might impact the aggressive behavior and radioresistance of cervical cancer stemness cells through bindingwith Rad21.