en Radiation Biology Radiation Biology تحقيق بديع Original Research <div style="text-align: justify;"><span style="font-size:10pt"><span style="text-justify:newspaper"><span style="text-kashida-space:50%"><span style="line-height:119%"><span style="font-family:Calibri"><span style="color:black"><span lang="en-US" style="font-size:9.0pt"><span style="font-family:Calibri"><span style="color:#1f497d"><span style="font-style:italic"><span style="font-weight:bold"><span style="language:en-US">Background:</span></span></span></span></span></span> <span lang="en-GB" style="font-size:9.0pt"><span style="font-family:Calibri"><span style="color:black"><span style="language:en-GB">This study investigates the mechanism by which the natural flavonoid drug Nodakenin intervenes in the phenotype of non-small cell lung cancer (NSCLC) by inhibiting the aurora kinase A-C-X-C motif chemokine ligand 5 (AURKA-CXCL5) axis, and analyses its role in enhancing tumour sensitivity to radiotherapy. </span></span></span></span><span lang="en-GB" style="font-size:9.0pt"><span style="font-family:Calibri"><span style="color:#1f497d"><span style="font-style:italic"><span style="font-weight:bold"><span style="language:en-GB">Materials and Methods: </span></span></span></span></span></span><span lang="en-GB" style="font-size:9.0pt"><span style="font-family:Calibri"><span style="color:black"><span style="language:en-GB">Human NSCLC A549 cells were classified into control group (CG), radiation group (RG), and Nodakenin group (NG). Radiotherapy was delivered at 2 Gy/day for five days using 6 MV X-rays. Nodakenin (10 </span></span></span></span><span lang="el" style="font-size:9.0pt"><span style="font-family:Calibri"><span style="color:black"><span style="language:el">&mu;</span></span></span></span><span lang="en-US" style="font-size:9.0pt"><span style="font-family:Calibri"><span style="color:black"><span style="language:en-US">M) was applied for 24 h after irradiation. Cell proliferation and survival were assessed using the MTT assay and the colony formation assay. Apoptosis was assessed by Annexin V-FITC/PI staining and flow cytometry. Gene expression of AURKA and CXCL5 was quantified by quantitative polymerase chain reaction (qPCR), DNA damage by </span></span></span></span><span lang="el" style="font-size:9.0pt"><span style="font-family:Calibri"><span style="color:black"><span style="language:el">&gamma;-</span></span></span></span><span lang="en-US" style="font-size:9.0pt"><span style="font-family:Calibri"><span style="color:black"><span style="language:en-US">H2AX immunofluorescence, and apoptotic proteins by Western blotting. </span></span></span></span><span lang="en-US" style="font-size:9.0pt"><span style="font-family:Calibri"><span style="color:#1f497d"><span style="font-style:italic"><span style="font-weight:bold"><span style="language:en-US">Results: </span></span></span></span></span></span><span lang="en-US" style="font-size:9.0pt"><span style="font-family:Calibri"><span style="color:black"><span style="language:en-US">The AURKA/CXCL5 mRNA in the RG surpassed that observed in the CG (P<0.05), while the AURKA/CXCL5 mRNA in the NG was lower than RG (P<0.05). The </span></span></span></span><span lang="el" style="font-size:9.0pt"><span style="font-family:Calibri"><span style="color:black"><span style="language:el">&gamma;-</span></span></span></span><span lang="en-US" style="font-size:9.0pt"><span style="font-family:Calibri"><span style="color:black"><span style="language:en-US">H2AX in the NG exceeded that in the RG. The cell viability in the NG was below that in the RG (P<0.05), and the apoptosis rate in the NG exceeded that in the RG (P<0.05). The quantity of cell migration and invasion in the NG was lower than RG (P<0.05). The Bax and caspase-3 proteins in the NG exceeded that in the RG (P<0.05), while the Bcl-2 was lower (P<0.05). </span></span></span></span><span lang="en-US" style="font-size:9.0pt"><span style="font-family:Calibri"><span style="color:#1f497d"><span style="font-style:italic"><span style="font-weight:bold"><span style="language:en-US">Conclusion: </span></span></span></span></span></span><span lang="en-US" style="font-size:9.0pt"><span style="font-family:Calibri"><span style="color:black"><span style="language:en-US">Nodakenin exacerbates DNA damage and apoptosis by inhibiting the AURKA-CXCL5 axis, thereby suppressing tumor cell proliferation and invasion.</span></span></span></span></span></span></span></span></span></span></div> Nodakenin, AURKA-CXCL5, NSCLC, DNA damage repair, neoplastic cell phenotype, aurora kinase A. 69 74 http://ijrr.com/browse.php?a_code=A-10-1-1457&slc_lang=en&sid=1 X. Wang 7900319475328460032761 7900319475328460032761 No Department of Western Medicine Pharmacy, Baoding No. 1 Central Hospital, Baoding, China R. Tian 7900319475328460032762 7900319475328460032762 No Department of Oncology, Hospital of the People's Liberation Army, 82nd Group Army, Baoding, China K. Duan 7900319475328460032763 7900319475328460032763 No General Surgery, Sanhe City Hospital in Hebei Province, Sanhe, China X. Zhang xuzhang0312@163.com 7900319475328460032764 7900319475328460032764 Yes Department of Ultrasound, Affiliated Hospital of Hebei University, Baoding, China