Knockdown of lncRNA FOXD1-AS1 promotes the radiosensitivity of lung squamous cell carcinoma cells by regulating the miR-4801/PUM1 axis

Radiation resistance is a main obstacle for clinical treatment of lung squamous cell carcinoma (LUSC). Recent studies have demonstrated that long noncoding RNA (lncRNA) can participate in LUSC tumorigenesis and radiosensitivity. The current study explored the role and mechanism of lncRNA FOXD1-AS1 in mediating radi-oresistance of LUSC cells. Expression levels of FOXD1-AS1, miR-4801 and pumilio RNA binding family member 1 (PUM1) in LUSC cell lines were estimated by RT-qPCR. PUM1 protein expression in cells were quantified by western blotting. CCK-8 and colony formation assays were conducted to measure LUSC cell viability and pro-liferation, respectively. TUNEL assays were used to analyze LUSC cell apoptosis. Subcellular localization of FOXD1-AS1 was determined via subcellular fractionation assay. The regulatory relationship among FOXD1-AS1, miR-4801 and PUM1 was verified by RNA pulldown assay, luciferase reporter assay and RNA immunoprecipi-tation assay.LncRNA FOXD1-AS1 was upregulated in LUSC cells. Knockdown of FOXD1-AS1 affected LUSC cell biological behaviors before and after radiation, including suppressing cell proliferation and promoting apoptosis. Moreover, silencing FOXD1-AS1 significantly promoted the radiosensitivity of LUSC cell lines, as evidenced by further inhibited cell proliferative ability and greatly enhanced apoptotic rate in the experimental group received ra-diation treatment and FOXD1-AS1 knockdown. In addition, FOXD1-AS1 bound with miR-4801 that targeted PUM1. PUM1 was also upregulated in LUSC cells. PUM1 overexpression reversed the promoting impact of FOXD1-AS1 depletion on LUSC cell radiosensitivity. Overall, silencing of FOXD1-AS1 promotes the radiosensi-tivity of LUSC cells via the miR-4801/PUM1 axis.