Glycitin exerts anticancer effect on human lung cancer cells through induction of apoptosis, cell cycle arrest, and inhibition of PI3K/AKT signal pathway

  • Yajuan Zhang
  • Rui Guo
  • Yan Wang
Keywords: Lung cancer, Isoflavones, Glycitin, Apoptosis, Cell cycle, PI3K/AKT signaling

Abstract

Purpose: To determine the effect of glycitin on PI3K/AKT signaling, migration, invasion, apoptosis, and cell cycle in A549 lung cancer cells.
Methods: 3-[4,5-Dimethylthiazole-2-yl]-2,5-diphenyltetrazolium bromide (MTT) and clonogenic assays were used to determine the proliferation and colony generation potency of A549 cells, respectively, after treatment with glycitin (0 - 120 μM). Apoptosis in A549 cells was measured using DAPI and Annexin V/PI-FITC assays. Cell cycle arrest was assessed byflow cytometry, while the effect of glycitin on migration and invasion of A549 cells was determined by Transwell assay. The effect of glycitin on expressions of proteins associated with PI3K/AKT signaling in A549 cells was measured using western blotting.
Results: Glycitin significantly inhibited the proliferation and colony generation potential of A549 cells (p < 0.05). The antiproliferative effects of glycitin on A549 cells were mediated through stimulation of apoptosis and cell cycle arrest at G0/G1-phase. The compound also distorted normal cellular morphology by causing membrane damage and nuclear fragmentation. The proportion of cells in the G0/G1-phase increased after glycitin treatment, when compared to the other two phases, demonstrating cell cycle arrest (p < 0.05). Glycitin suppressed the migration and invasion of A549 cells. However, Western blotting results showed that glycitin down-regulated the expressions of PI3K/AKT signaling proteins in A549 cells (p < 0.05).
Conclusion: Glycitin produced significant anticancer effect on A549 cells via enhanced apoptosis, induction of cell cycle arrest, and inhibition of PI3K/AKT signalling. Moreover, it suppressed the migration and invasion of A549 cells. Therefore, glycitin is a potential lead molecule for the development of a therapeutic agent for invasive lung cancer.

Published
2022-06-17
Section
Articles

Journal Identifiers


eISSN: 1596-9827
print ISSN: 1596-5996