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IJPER · Lens · Anticancer, Apoptotic, Cell Migration and Invasion Inhibition and in silico Molecular Docking Studies of Naringetol in A-549 Human Lung Cancer Cells

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Article · Volume 59, Issue 1 · pp. 221–229

Anticancer, Apoptotic, Cell Migration and Invasion Inhibition and in silico Molecular Docking Studies of Naringetol in A-549 Human Lung Cancer Cells

Jing Li1, Beishou Wu2, Xuejun Huang3, Weizhong Tang4

  1. 1Department of Respiratory and Critical Care Medicine, Wuhan Third Hospital Tongren Hospital of Wuhan University, Wuhan Hubei, CHINA.
  2. 2Department of Respiratory Medicine, Nanxiang Branch of Ruijin Hospital, Shanghai, CHINA.
  3. 3Department of Outpatient, the General Hospital of Western Theater Command of Chinese People’s Liberation Army, Chengdu Sichuan, CHINA.
  4. 4Department of Hematology Oncology, Changzhou No.7 People’ s HospitaI, Changzhou Jiangsu, CHINA.

Abstract

Aims The main objective of this research work was to investigate the anticancer effects of Naringetol in A-549 human lung cancer cells along with evaluating its effects on cell apoptosis, cell migration and cell invasion and decoding the molecular mechanism of action by studying interactions of this molecule with the target protein using in silico molecular docking studies. Materials and Methods MTT assay was used to study effects on cell viability while as effects on cell colony was evaluated by clonogenic assay. Acridine orange/ethidium bromide, DAPI staining assays using fluorescence microscopy were used to study effects on cell apoptosis. Cell migration and cell invasion inhibition was evaluated by Transwell assay. AutoDoc Vina software used to carry out docking simulation studies using Naringetol and EGFR (epidermal growth factor receptor) protein. Results Results indicated that Naringetol induced dose and time-dependent inhibition of A-549 cancer cell viability along with inhibiting cell colony formation. Fluorescence microscopy revealed that naringetol molecule induced apoptosis like features in A-549 cells including nuclear and chromatin condensation and deformed cell membrane structures. Naringetol also led to a significant inhibition of cell migration and invasion hinting to its anti-metastatic potency. Molecular docking simulation studies indicated potential binding of naringetol with the key amino acid residues of the EGFR target protein with a binding score of -8.5 kcal/mole. Conclusion In conclusion, these results reveal that naringetol inhibits lung cancer cell proliferation through the induction of cell apoptosis and suppression of cell migration and cell invasion. The target protein involved might be the EGFR protein as revealed by in silico molecular docking simulation studies.

Keywords: Naringetol; Lung cancer; Cell apoptosis; Cell migration; Cell invasion

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