Cargando…
Autophagy and apoptosis induction by sesamin in MOLT-4 and NB4 leukemia cells
Sesamin, the major furofuran lignan found in the seeds of Sesamum indicum L., has been investigated for its various medicinal properties. In the present study, the anti-leukemic effects of sesamin and its underlying mechanisms were investigated in MOLT-4 and NB4 acute leukemic cells. Leukemic cells...
Autores principales: | , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7693381/ https://www.ncbi.nlm.nih.gov/pubmed/33262824 http://dx.doi.org/10.3892/ol.2020.12293 |
_version_ | 1783614730953293824 |
---|---|
author | Deesrisak, Kamolchanok Chatupheeraphat, Chawalit Roytrakul, Sittiruk Anurathapan, Usanarat Tanyong, Dalina |
author_facet | Deesrisak, Kamolchanok Chatupheeraphat, Chawalit Roytrakul, Sittiruk Anurathapan, Usanarat Tanyong, Dalina |
author_sort | Deesrisak, Kamolchanok |
collection | PubMed |
description | Sesamin, the major furofuran lignan found in the seeds of Sesamum indicum L., has been investigated for its various medicinal properties. In the present study, the anti-leukemic effects of sesamin and its underlying mechanisms were investigated in MOLT-4 and NB4 acute leukemic cells. Leukemic cells were treated with various concentrations of sesamin. Cell viability was determined using an MTT assay. Flow cytometry using Annexin V-FITC/PI staining and anti-LC3/FITC antibodies was applied to detect the level of apoptosis and autophagy, respectively. Reverse transcription-quantitative PCR was performed to examine the alterations in the mRNA expression of apoptotic and autophagic genes. In addition, bioinformatics tools were used to predict the possible interactions between sesamin and its targets. The results revealed that sesamin inhibited MOLT-4 and NB4 cell proliferation in a dose-dependent manner. In addition, sesamin induced both apoptosis and autophagy. In sesamin-treated cells, the gene expression levels of caspase 3 and unc-51 like autophagy activating kinase 1 (ULK1) were upregulated, while those of mTOR were downregulated compared with in the control. Notably, the protein-chemical interaction network indicated that caspase 3, mTOR and ULK1 were the essential factors involved in the effects of sesamin treatment, as with anticancer agents, such as rapamycin, AZD8055, Torin1 and 2. Overall, the findings of the present study suggested that sesamin inhibited MOLT-4 and NB4 cell proliferation, and induced apoptosis and autophagy through the regulation of caspase 3 and mTOR/ULK1 signaling, respectively. |
format | Online Article Text |
id | pubmed-7693381 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-76933812020-11-30 Autophagy and apoptosis induction by sesamin in MOLT-4 and NB4 leukemia cells Deesrisak, Kamolchanok Chatupheeraphat, Chawalit Roytrakul, Sittiruk Anurathapan, Usanarat Tanyong, Dalina Oncol Lett Articles Sesamin, the major furofuran lignan found in the seeds of Sesamum indicum L., has been investigated for its various medicinal properties. In the present study, the anti-leukemic effects of sesamin and its underlying mechanisms were investigated in MOLT-4 and NB4 acute leukemic cells. Leukemic cells were treated with various concentrations of sesamin. Cell viability was determined using an MTT assay. Flow cytometry using Annexin V-FITC/PI staining and anti-LC3/FITC antibodies was applied to detect the level of apoptosis and autophagy, respectively. Reverse transcription-quantitative PCR was performed to examine the alterations in the mRNA expression of apoptotic and autophagic genes. In addition, bioinformatics tools were used to predict the possible interactions between sesamin and its targets. The results revealed that sesamin inhibited MOLT-4 and NB4 cell proliferation in a dose-dependent manner. In addition, sesamin induced both apoptosis and autophagy. In sesamin-treated cells, the gene expression levels of caspase 3 and unc-51 like autophagy activating kinase 1 (ULK1) were upregulated, while those of mTOR were downregulated compared with in the control. Notably, the protein-chemical interaction network indicated that caspase 3, mTOR and ULK1 were the essential factors involved in the effects of sesamin treatment, as with anticancer agents, such as rapamycin, AZD8055, Torin1 and 2. Overall, the findings of the present study suggested that sesamin inhibited MOLT-4 and NB4 cell proliferation, and induced apoptosis and autophagy through the regulation of caspase 3 and mTOR/ULK1 signaling, respectively. D.A. Spandidos 2021-01 2020-11-12 /pmc/articles/PMC7693381/ /pubmed/33262824 http://dx.doi.org/10.3892/ol.2020.12293 Text en Copyright: © Deesrisak 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 Deesrisak, Kamolchanok Chatupheeraphat, Chawalit Roytrakul, Sittiruk Anurathapan, Usanarat Tanyong, Dalina Autophagy and apoptosis induction by sesamin in MOLT-4 and NB4 leukemia cells |
title | Autophagy and apoptosis induction by sesamin in MOLT-4 and NB4 leukemia cells |
title_full | Autophagy and apoptosis induction by sesamin in MOLT-4 and NB4 leukemia cells |
title_fullStr | Autophagy and apoptosis induction by sesamin in MOLT-4 and NB4 leukemia cells |
title_full_unstemmed | Autophagy and apoptosis induction by sesamin in MOLT-4 and NB4 leukemia cells |
title_short | Autophagy and apoptosis induction by sesamin in MOLT-4 and NB4 leukemia cells |
title_sort | autophagy and apoptosis induction by sesamin in molt-4 and nb4 leukemia cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7693381/ https://www.ncbi.nlm.nih.gov/pubmed/33262824 http://dx.doi.org/10.3892/ol.2020.12293 |
work_keys_str_mv | AT deesrisakkamolchanok autophagyandapoptosisinductionbysesamininmolt4andnb4leukemiacells AT chatupheeraphatchawalit autophagyandapoptosisinductionbysesamininmolt4andnb4leukemiacells AT roytrakulsittiruk autophagyandapoptosisinductionbysesamininmolt4andnb4leukemiacells AT anurathapanusanarat autophagyandapoptosisinductionbysesamininmolt4andnb4leukemiacells AT tanyongdalina autophagyandapoptosisinductionbysesamininmolt4andnb4leukemiacells |