Vitexin induces apoptosis through mitochondrial pathway and PI3K/Akt/mTOR signaling in human non-small cell lung cancer A549 cells

Vitexin induces apoptosis through mitochondrial pathway and PI3K/Akt/mTOR signaling in human non-small cell lung cancer A549 cells

Abstract Background: Currently, the prognosis of patients with non-small cell lung cancer (NSCLC) remains dismal; hence, it is critical to identify effective anti-NSCLC agents with limited side effects. This study aimed to evaluate the therapeutic potential of flavonoid compound vitexin in human NSCLC cells and the underlying mechanisms. Results: The experimental results indicated that vitexin reduced the viability of A549 cells in a dose-dependent manner with nearly no toxicity against normal human bronchial epithelial 16HBE cells. Vitexin also dose-dependently increased A549 cell apoptosis, accompanied by the decreased Bcl-2/Bax ratio and the increased expression of cleaved caspase-3. Moreover, the in vivo anticancer activity of vitexin was further determined in nude mice bearing A549 cells. In addition, vitexin induced the release of cytochrome c from the mitochondria to the cytosol and the loss of mitochondrial membrane potential. Vitexin also significantly reduced the levels of p-PI3K, p-Akt and p-mTOR, and the pro-apoptotic effect of vitexin on A549 cells was partly blocked by SC79, an Akt activator. Conclusions: Accordingly, we believed that vitexin could be used as a potential therapeutic agent for the treatment of NSCLC in the future.

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Main Authors: Liu,Xiaoli, Jiang,Qingfeng, Liu,Huaimin, Luo,Suxia
Format: Digital revista
Language:English
Published: Sociedad de Biología de Chile 2019
Online Access:http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602019000100206
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spelling oai:scielo:S0716-976020190001002062019-10-10Vitexin induces apoptosis through mitochondrial pathway and PI3K/Akt/mTOR signaling in human non-small cell lung cancer A549 cellsLiu,XiaoliJiang,QingfengLiu,HuaiminLuo,Suxia Non-small cell lung cancer Vitexin Mitochondrial dysfunction PI3K/Akt/mTOR signaling Abstract Background: Currently, the prognosis of patients with non-small cell lung cancer (NSCLC) remains dismal; hence, it is critical to identify effective anti-NSCLC agents with limited side effects. This study aimed to evaluate the therapeutic potential of flavonoid compound vitexin in human NSCLC cells and the underlying mechanisms. Results: The experimental results indicated that vitexin reduced the viability of A549 cells in a dose-dependent manner with nearly no toxicity against normal human bronchial epithelial 16HBE cells. Vitexin also dose-dependently increased A549 cell apoptosis, accompanied by the decreased Bcl-2/Bax ratio and the increased expression of cleaved caspase-3. Moreover, the in vivo anticancer activity of vitexin was further determined in nude mice bearing A549 cells. In addition, vitexin induced the release of cytochrome c from the mitochondria to the cytosol and the loss of mitochondrial membrane potential. Vitexin also significantly reduced the levels of p-PI3K, p-Akt and p-mTOR, and the pro-apoptotic effect of vitexin on A549 cells was partly blocked by SC79, an Akt activator. Conclusions: Accordingly, we believed that vitexin could be used as a potential therapeutic agent for the treatment of NSCLC in the future.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.52 20192019-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602019000100206en10.1186/s40659-019-0214-y
institution SCIELO
collection OJS
country Chile
countrycode CL
component Revista
access En linea
databasecode rev-scielo-cl
tag revista
region America del Sur
libraryname SciELO
language English
format Digital
author Liu,Xiaoli
Jiang,Qingfeng
Liu,Huaimin
Luo,Suxia
spellingShingle Liu,Xiaoli
Jiang,Qingfeng
Liu,Huaimin
Luo,Suxia
Vitexin induces apoptosis through mitochondrial pathway and PI3K/Akt/mTOR signaling in human non-small cell lung cancer A549 cells
author_facet Liu,Xiaoli
Jiang,Qingfeng
Liu,Huaimin
Luo,Suxia
author_sort Liu,Xiaoli
title Vitexin induces apoptosis through mitochondrial pathway and PI3K/Akt/mTOR signaling in human non-small cell lung cancer A549 cells
title_short Vitexin induces apoptosis through mitochondrial pathway and PI3K/Akt/mTOR signaling in human non-small cell lung cancer A549 cells
title_full Vitexin induces apoptosis through mitochondrial pathway and PI3K/Akt/mTOR signaling in human non-small cell lung cancer A549 cells
title_fullStr Vitexin induces apoptosis through mitochondrial pathway and PI3K/Akt/mTOR signaling in human non-small cell lung cancer A549 cells
title_full_unstemmed Vitexin induces apoptosis through mitochondrial pathway and PI3K/Akt/mTOR signaling in human non-small cell lung cancer A549 cells
title_sort vitexin induces apoptosis through mitochondrial pathway and pi3k/akt/mtor signaling in human non-small cell lung cancer a549 cells
description Abstract Background: Currently, the prognosis of patients with non-small cell lung cancer (NSCLC) remains dismal; hence, it is critical to identify effective anti-NSCLC agents with limited side effects. This study aimed to evaluate the therapeutic potential of flavonoid compound vitexin in human NSCLC cells and the underlying mechanisms. Results: The experimental results indicated that vitexin reduced the viability of A549 cells in a dose-dependent manner with nearly no toxicity against normal human bronchial epithelial 16HBE cells. Vitexin also dose-dependently increased A549 cell apoptosis, accompanied by the decreased Bcl-2/Bax ratio and the increased expression of cleaved caspase-3. Moreover, the in vivo anticancer activity of vitexin was further determined in nude mice bearing A549 cells. In addition, vitexin induced the release of cytochrome c from the mitochondria to the cytosol and the loss of mitochondrial membrane potential. Vitexin also significantly reduced the levels of p-PI3K, p-Akt and p-mTOR, and the pro-apoptotic effect of vitexin on A549 cells was partly blocked by SC79, an Akt activator. Conclusions: Accordingly, we believed that vitexin could be used as a potential therapeutic agent for the treatment of NSCLC in the future.
publisher Sociedad de Biología de Chile
publishDate 2019
url http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602019000100206
work_keys_str_mv AT liuxiaoli vitexininducesapoptosisthroughmitochondrialpathwayandpi3kaktmtorsignalinginhumannonsmallcelllungcancera549cells
AT jiangqingfeng vitexininducesapoptosisthroughmitochondrialpathwayandpi3kaktmtorsignalinginhumannonsmallcelllungcancera549cells
AT liuhuaimin vitexininducesapoptosisthroughmitochondrialpathwayandpi3kaktmtorsignalinginhumannonsmallcelllungcancera549cells
AT luosuxia vitexininducesapoptosisthroughmitochondrialpathwayandpi3kaktmtorsignalinginhumannonsmallcelllungcancera549cells
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