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Nanocurcumin-Mediated Down-Regulation of Telomerase Via Stimulating TGFβ1 Signaling Pathway in Hepatocellular Carcinoma Cells

BACKGROUND: Curcumin, extracted from turmeric, represents enormous potential to serve as an anticancer agent. Telomerase is viewed as a prominent molecular target of curcumin, and transforming growth factor-β1 (TGFβ1) has proven to be a major inhibitory signaling pathway for telomerase activity. In...

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Autores principales: Shariati, Molood, Hajigholami, Samira, Malekshahi, Ziba Veisi, Entezari, Maliheh, Bodaghabadi, Narges, Sadeghizadeh, Majid
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Pasteur Institute 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5889502/
https://www.ncbi.nlm.nih.gov/pubmed/28992682
http://dx.doi.org/10.22034/ibj.22.3.171
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author Shariati, Molood
Hajigholami, Samira
Malekshahi, Ziba Veisi
Entezari, Maliheh
Bodaghabadi, Narges
Sadeghizadeh, Majid
author_facet Shariati, Molood
Hajigholami, Samira
Malekshahi, Ziba Veisi
Entezari, Maliheh
Bodaghabadi, Narges
Sadeghizadeh, Majid
author_sort Shariati, Molood
collection PubMed
description BACKGROUND: Curcumin, extracted from turmeric, represents enormous potential to serve as an anticancer agent. Telomerase is viewed as a prominent molecular target of curcumin, and transforming growth factor-β1 (TGFβ1) has proven to be a major inhibitory signaling pathway for telomerase activity. In the current study, we aimed to explore suppressive effects of nanocurcumin on telomerase expression through TGFβ1 pathway in a hepatocellular carcinoma cell line (Huh7). METHODS: MTT assay was used to determine the effect of nonocurcumin on viability of Huh7 cells. RT-PCR was used to analyze the gene expression patterns. RESULTS: MTT assay revealed that nanocurcumin acts in a dose- and time-dependent manner to diminish the cell viability. RT-PCR analysis indicated that nanocurcumin results in augmentation of TGFβ1 72 hours post treatment and leads to the reduction of telomerase expression 48 and 72 hours post exposure. Also, up-regulation of Smad3 and E2F1 and down-regulation of Smad7 confirmed the effect of nanocurcumin on intermediate components of TGFβ1 pathway. Furthermore, transfection of the proximal promoter of telomerase triggered a significant reduction in luciferase activity. CONCLUSION: The data from the present study lead us to develop a deeper understanding of the mechanisms underlying nanocurcumin-mediated regulation of telomerase expression, thereby presenting a new perspective to the landscape of using nanocurcumin as a cancer-oriented therapeutic agent.
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spelling pubmed-58895022018-05-01 Nanocurcumin-Mediated Down-Regulation of Telomerase Via Stimulating TGFβ1 Signaling Pathway in Hepatocellular Carcinoma Cells Shariati, Molood Hajigholami, Samira Malekshahi, Ziba Veisi Entezari, Maliheh Bodaghabadi, Narges Sadeghizadeh, Majid Iran Biomed J Full Length BACKGROUND: Curcumin, extracted from turmeric, represents enormous potential to serve as an anticancer agent. Telomerase is viewed as a prominent molecular target of curcumin, and transforming growth factor-β1 (TGFβ1) has proven to be a major inhibitory signaling pathway for telomerase activity. In the current study, we aimed to explore suppressive effects of nanocurcumin on telomerase expression through TGFβ1 pathway in a hepatocellular carcinoma cell line (Huh7). METHODS: MTT assay was used to determine the effect of nonocurcumin on viability of Huh7 cells. RT-PCR was used to analyze the gene expression patterns. RESULTS: MTT assay revealed that nanocurcumin acts in a dose- and time-dependent manner to diminish the cell viability. RT-PCR analysis indicated that nanocurcumin results in augmentation of TGFβ1 72 hours post treatment and leads to the reduction of telomerase expression 48 and 72 hours post exposure. Also, up-regulation of Smad3 and E2F1 and down-regulation of Smad7 confirmed the effect of nanocurcumin on intermediate components of TGFβ1 pathway. Furthermore, transfection of the proximal promoter of telomerase triggered a significant reduction in luciferase activity. CONCLUSION: The data from the present study lead us to develop a deeper understanding of the mechanisms underlying nanocurcumin-mediated regulation of telomerase expression, thereby presenting a new perspective to the landscape of using nanocurcumin as a cancer-oriented therapeutic agent. Pasteur Institute 2018-05 /pmc/articles/PMC5889502/ /pubmed/28992682 http://dx.doi.org/10.22034/ibj.22.3.171 Text en Copyright: © Iranian Biomedical Journal http://creativecommons.org/licenses/by/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Full Length
Shariati, Molood
Hajigholami, Samira
Malekshahi, Ziba Veisi
Entezari, Maliheh
Bodaghabadi, Narges
Sadeghizadeh, Majid
Nanocurcumin-Mediated Down-Regulation of Telomerase Via Stimulating TGFβ1 Signaling Pathway in Hepatocellular Carcinoma Cells
title Nanocurcumin-Mediated Down-Regulation of Telomerase Via Stimulating TGFβ1 Signaling Pathway in Hepatocellular Carcinoma Cells
title_full Nanocurcumin-Mediated Down-Regulation of Telomerase Via Stimulating TGFβ1 Signaling Pathway in Hepatocellular Carcinoma Cells
title_fullStr Nanocurcumin-Mediated Down-Regulation of Telomerase Via Stimulating TGFβ1 Signaling Pathway in Hepatocellular Carcinoma Cells
title_full_unstemmed Nanocurcumin-Mediated Down-Regulation of Telomerase Via Stimulating TGFβ1 Signaling Pathway in Hepatocellular Carcinoma Cells
title_short Nanocurcumin-Mediated Down-Regulation of Telomerase Via Stimulating TGFβ1 Signaling Pathway in Hepatocellular Carcinoma Cells
title_sort nanocurcumin-mediated down-regulation of telomerase via stimulating tgfβ1 signaling pathway in hepatocellular carcinoma cells
topic Full Length
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5889502/
https://www.ncbi.nlm.nih.gov/pubmed/28992682
http://dx.doi.org/10.22034/ibj.22.3.171
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