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Garlic-derived compound S-allylmercaptocysteine inhibits cell growth and induces apoptosis via the JNK and p38 pathways in human colorectal carcinoma cells

S-allylmercaptocysteine (SAMC) is an active compound that is derived from garlic and has been demonstrated to possess antitumor properties in vitro. The present study aimed to investigate the effect of SAMC and determine the underlying mechanism of this effect on human colorectal carcinoma cells. Th...

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Autores principales: ZHANG, YAN, LI, HONG-YAN, ZHANG, ZHI-HUA, BIAN, HONG-LEI, LIN, GUI
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4214450/
https://www.ncbi.nlm.nih.gov/pubmed/25364433
http://dx.doi.org/10.3892/ol.2014.2579
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author ZHANG, YAN
LI, HONG-YAN
ZHANG, ZHI-HUA
BIAN, HONG-LEI
LIN, GUI
author_facet ZHANG, YAN
LI, HONG-YAN
ZHANG, ZHI-HUA
BIAN, HONG-LEI
LIN, GUI
author_sort ZHANG, YAN
collection PubMed
description S-allylmercaptocysteine (SAMC) is an active compound that is derived from garlic and has been demonstrated to possess antitumor properties in vitro. The present study aimed to investigate the effect of SAMC and determine the underlying mechanism of this effect on human colorectal carcinoma cells. The SW620 cells were cultured with various concentrations of SAMC and cell viability was detected using an MTT assay. Analysis of apoptosis was performed using terminal deoxynucleotidyl-transferase-mediated deoxyuridine triphosphate nick end labeling. The c-Jun N-terminal kinase (JNK) and p38 mitogen activated protein kinase (p38) signaling pathways were investigated by polymerase chain reaction. SAMC was observed to reduce cell viability in a dose- and time-dependent manner, partially through the induction of apoptosis in human colorectal carcinoma cells. At the molecular level, SAMC induces apoptosis through JNK and p38 signaling pathways, increasing tumor protein p53 (p53) and Bax activation in the SW620 cells. The most effective concentration of SAMC for the induction of SW620 cell apoptosis was found to be 400 μM, which was confirmed through cell viability assays and apoptosis analysis. The current study indicated that SAMC inhibits cell proliferation and induces apoptosis of SW620 cells via the JNK and p38 pathways. The results from the current study demonstrated that SAMC must be further investigated as a novel preventive or therapeutic agent for the treatment of colorectal carcinoma, and potentially for use in other tumor types.
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spelling pubmed-42144502014-10-31 Garlic-derived compound S-allylmercaptocysteine inhibits cell growth and induces apoptosis via the JNK and p38 pathways in human colorectal carcinoma cells ZHANG, YAN LI, HONG-YAN ZHANG, ZHI-HUA BIAN, HONG-LEI LIN, GUI Oncol Lett Articles S-allylmercaptocysteine (SAMC) is an active compound that is derived from garlic and has been demonstrated to possess antitumor properties in vitro. The present study aimed to investigate the effect of SAMC and determine the underlying mechanism of this effect on human colorectal carcinoma cells. The SW620 cells were cultured with various concentrations of SAMC and cell viability was detected using an MTT assay. Analysis of apoptosis was performed using terminal deoxynucleotidyl-transferase-mediated deoxyuridine triphosphate nick end labeling. The c-Jun N-terminal kinase (JNK) and p38 mitogen activated protein kinase (p38) signaling pathways were investigated by polymerase chain reaction. SAMC was observed to reduce cell viability in a dose- and time-dependent manner, partially through the induction of apoptosis in human colorectal carcinoma cells. At the molecular level, SAMC induces apoptosis through JNK and p38 signaling pathways, increasing tumor protein p53 (p53) and Bax activation in the SW620 cells. The most effective concentration of SAMC for the induction of SW620 cell apoptosis was found to be 400 μM, which was confirmed through cell viability assays and apoptosis analysis. The current study indicated that SAMC inhibits cell proliferation and induces apoptosis of SW620 cells via the JNK and p38 pathways. The results from the current study demonstrated that SAMC must be further investigated as a novel preventive or therapeutic agent for the treatment of colorectal carcinoma, and potentially for use in other tumor types. D.A. Spandidos 2014-12 2014-09-30 /pmc/articles/PMC4214450/ /pubmed/25364433 http://dx.doi.org/10.3892/ol.2014.2579 Text en Copyright © 2014, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Articles
ZHANG, YAN
LI, HONG-YAN
ZHANG, ZHI-HUA
BIAN, HONG-LEI
LIN, GUI
Garlic-derived compound S-allylmercaptocysteine inhibits cell growth and induces apoptosis via the JNK and p38 pathways in human colorectal carcinoma cells
title Garlic-derived compound S-allylmercaptocysteine inhibits cell growth and induces apoptosis via the JNK and p38 pathways in human colorectal carcinoma cells
title_full Garlic-derived compound S-allylmercaptocysteine inhibits cell growth and induces apoptosis via the JNK and p38 pathways in human colorectal carcinoma cells
title_fullStr Garlic-derived compound S-allylmercaptocysteine inhibits cell growth and induces apoptosis via the JNK and p38 pathways in human colorectal carcinoma cells
title_full_unstemmed Garlic-derived compound S-allylmercaptocysteine inhibits cell growth and induces apoptosis via the JNK and p38 pathways in human colorectal carcinoma cells
title_short Garlic-derived compound S-allylmercaptocysteine inhibits cell growth and induces apoptosis via the JNK and p38 pathways in human colorectal carcinoma cells
title_sort garlic-derived compound s-allylmercaptocysteine inhibits cell growth and induces apoptosis via the jnk and p38 pathways in human colorectal carcinoma cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4214450/
https://www.ncbi.nlm.nih.gov/pubmed/25364433
http://dx.doi.org/10.3892/ol.2014.2579
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