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Mechanism by which nodakenin inhibits the AURKA-CXCL5 axis to intervene in the phenotype of non-small cell lung cancer
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X. Wang   , R. Tian , K. Duan , X. Zhang |
| Department of Ultrasound, Affiliated Hospital of Hebei University, Baoding, China , xuzhang0312@163.com |
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Abstract: (535 Views) |
Background: 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. Materials and Methods: 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 μM) 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 γ-H2AX immunofluorescence, and apoptotic proteins by Western blotting. Results: 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 γ-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). Conclusion: Nodakenin exacerbates DNA damage and apoptosis by inhibiting the AURKA-CXCL5 axis, thereby suppressing tumor cell proliferation and invasion. |
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| Keywords: Nodakenin, AURKA-CXCL5, NSCLC, DNA damage repair, neoplastic cell phenotype, aurora kinase A. |
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Full-Text [PDF 1017 kb]
(99 Downloads)
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Type of Study: Original Research |
Subject:
Radiation Biology
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