Cargando…

β-hydroxyisovaleryl-shikonin induces human cervical cancer cell apoptosis via PI3K/AKT/mTOR signaling

The present study aimed to investigate the inhibitory ability of β-hydroxyisovaleryl-shikonin (β-HIVS) on the proliferation of human cervical cancer HeLa cells and to identify the mechanism of this effect. The HeLa cells were treated with β-HIVS and the inhibition of cell growth was detected by an M...

Descripción completa

Detalles Bibliográficos
Autores principales: LU, DAN, QIAN, JING, LI, WEI, FENG, QIANQIAN, PAN, SHU, ZHANG, SIQUAN
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4665374/
https://www.ncbi.nlm.nih.gov/pubmed/26788147
http://dx.doi.org/10.3892/ol.2015.3769
_version_ 1782403558907314176
author LU, DAN
QIAN, JING
LI, WEI
FENG, QIANQIAN
PAN, SHU
ZHANG, SIQUAN
author_facet LU, DAN
QIAN, JING
LI, WEI
FENG, QIANQIAN
PAN, SHU
ZHANG, SIQUAN
author_sort LU, DAN
collection PubMed
description The present study aimed to investigate the inhibitory ability of β-hydroxyisovaleryl-shikonin (β-HIVS) on the proliferation of human cervical cancer HeLa cells and to identify the mechanism of this effect. The HeLa cells were treated with β-HIVS and the inhibition of cell growth was detected by an MTT assay. Flow cytometry was performed to analyze the apoptosis rate and cell cycle distribution of HeLa cells. Reverse transcription-polymerase chain reaction and western blot analysis were used to examine the expression of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway proteins. The results revealed that β-HIVS inhibited HeLa cell proliferation in a dose- and time-dependent manner. With the administration of increasing concentrations of β-HIVS, the apoptotic rate of HeLa cells was also increased. The cell cycle was slightly arrested at the S phase, with ~6% of cells in this phase, subsequent to treatment with 10 µM β-HIVS. In addition, β-HIVS markedly reduced the expression levels of PI3K, AKT, mTOR and 70-kDa ribosomal protein S6 kinase in HeLa cells. β-HIVS promoted cervical cancer cell apoptosis by inhibiting the PI3K/AKT/mTOR signaling pathway and suppressing downstream gene expression. The present study is expected to lead to the development of molecular targeted therapy for this signaling pathway as a novel method of cervical cancer treatment.
format Online
Article
Text
id pubmed-4665374
institution National Center for Biotechnology Information
language English
publishDate 2015
publisher D.A. Spandidos
record_format MEDLINE/PubMed
spelling pubmed-46653742016-01-19 β-hydroxyisovaleryl-shikonin induces human cervical cancer cell apoptosis via PI3K/AKT/mTOR signaling LU, DAN QIAN, JING LI, WEI FENG, QIANQIAN PAN, SHU ZHANG, SIQUAN Oncol Lett Articles The present study aimed to investigate the inhibitory ability of β-hydroxyisovaleryl-shikonin (β-HIVS) on the proliferation of human cervical cancer HeLa cells and to identify the mechanism of this effect. The HeLa cells were treated with β-HIVS and the inhibition of cell growth was detected by an MTT assay. Flow cytometry was performed to analyze the apoptosis rate and cell cycle distribution of HeLa cells. Reverse transcription-polymerase chain reaction and western blot analysis were used to examine the expression of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway proteins. The results revealed that β-HIVS inhibited HeLa cell proliferation in a dose- and time-dependent manner. With the administration of increasing concentrations of β-HIVS, the apoptotic rate of HeLa cells was also increased. The cell cycle was slightly arrested at the S phase, with ~6% of cells in this phase, subsequent to treatment with 10 µM β-HIVS. In addition, β-HIVS markedly reduced the expression levels of PI3K, AKT, mTOR and 70-kDa ribosomal protein S6 kinase in HeLa cells. β-HIVS promoted cervical cancer cell apoptosis by inhibiting the PI3K/AKT/mTOR signaling pathway and suppressing downstream gene expression. The present study is expected to lead to the development of molecular targeted therapy for this signaling pathway as a novel method of cervical cancer treatment. D.A. Spandidos 2015-12 2015-09-30 /pmc/articles/PMC4665374/ /pubmed/26788147 http://dx.doi.org/10.3892/ol.2015.3769 Text en Copyright: © Lu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
LU, DAN
QIAN, JING
LI, WEI
FENG, QIANQIAN
PAN, SHU
ZHANG, SIQUAN
β-hydroxyisovaleryl-shikonin induces human cervical cancer cell apoptosis via PI3K/AKT/mTOR signaling
title β-hydroxyisovaleryl-shikonin induces human cervical cancer cell apoptosis via PI3K/AKT/mTOR signaling
title_full β-hydroxyisovaleryl-shikonin induces human cervical cancer cell apoptosis via PI3K/AKT/mTOR signaling
title_fullStr β-hydroxyisovaleryl-shikonin induces human cervical cancer cell apoptosis via PI3K/AKT/mTOR signaling
title_full_unstemmed β-hydroxyisovaleryl-shikonin induces human cervical cancer cell apoptosis via PI3K/AKT/mTOR signaling
title_short β-hydroxyisovaleryl-shikonin induces human cervical cancer cell apoptosis via PI3K/AKT/mTOR signaling
title_sort β-hydroxyisovaleryl-shikonin induces human cervical cancer cell apoptosis via pi3k/akt/mtor signaling
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4665374/
https://www.ncbi.nlm.nih.gov/pubmed/26788147
http://dx.doi.org/10.3892/ol.2015.3769
work_keys_str_mv AT ludan bhydroxyisovalerylshikonininduceshumancervicalcancercellapoptosisviapi3kaktmtorsignaling
AT qianjing bhydroxyisovalerylshikonininduceshumancervicalcancercellapoptosisviapi3kaktmtorsignaling
AT liwei bhydroxyisovalerylshikonininduceshumancervicalcancercellapoptosisviapi3kaktmtorsignaling
AT fengqianqian bhydroxyisovalerylshikonininduceshumancervicalcancercellapoptosisviapi3kaktmtorsignaling
AT panshu bhydroxyisovalerylshikonininduceshumancervicalcancercellapoptosisviapi3kaktmtorsignaling
AT zhangsiquan bhydroxyisovalerylshikonininduceshumancervicalcancercellapoptosisviapi3kaktmtorsignaling