Piceatannol induced apoptosis through up-regulation of microRNA-181a in melanoma cells

Abstract Background Melanoma took top position among the lethal cancers and, despite there have been some great attempts made to increase the natural life of patients with metastatic disease, long-lasting and complete remissions are few. Piceatannol, owns the similar function as resveratrol, has be...

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Autores principales: Du,Maotao, Zhang,Zhong, Gao,Tao
Lenguaje:English
Publicado: Sociedad de Biología de Chile 2017
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Acceso en línea:http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602017000100226
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spelling oai:scielo:S0716-976020170001002262018-01-08Piceatannol induced apoptosis through up-regulation of microRNA-181a in melanoma cellsDu,MaotaoZhang,ZhongGao,Tao Piceatannol Apoptosis microRNA-181-a Melanoma cells Abstract Background Melanoma took top position among the lethal cancers and, despite there have been some great attempts made to increase the natural life of patients with metastatic disease, long-lasting and complete remissions are few. Piceatannol, owns the similar function as resveratrol, has been defined as an anti-cancer agent playing important role in inhibition of proliferation, migration and metastasis in various cancer. Thus, we aim to investigate the anti-cancer effect and mechanisms of piceatannol in melanoma cells. Methods Melanoma cell lines WM266-4 and A2058 were treated either with or without piceatannol. Cell viability and cell apoptosis were assessed by using MTT and Annexin V/PI assay, respectively. Cells were transfected with specific miRNA using Lipfectamine 2000. miRNA bingding ability to 3'-UTR region within specific gene was assed by firefly luciferase analysis. Gene and protein expression was eveluated by qRT-PCR and western blot analysis, respectively. Results Our study showed that piceatannol inhibited WM266-4 and A2058 cells growth and induced apoptosis. Totally, 16 differentially expressed miRNAs were screened out including 8 up-regulated and 8 down-regulated miRNAs. Expression level of miR-181a is significantly higher in piceatannol-treated cells than normal control and is lower in melanoma cancer tissues than its adjacent normal tissues. Bcl-2 is a target gene of miR-181a. Moreover, silencing of miR-181a reverses the decrease of cell viability induced by piceatannol in WM266-4 and A2058 cells. Taken together, present study uncovered the ability of piceatannol to repress melanoma cell growth and clarified the contribution of miR-181a in the anticancer role of piceatannol. Conclusion The present study proposes that piceatannol can be taken into account to be a hopeful anticancer agent for melanoma.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.50 20172017-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602017000100226en10.1186/s40659-017-0141-8
institution Scielo Chile
collection Scielo Chile
language English
topic Piceatannol
Apoptosis
microRNA-181-a
Melanoma cells
spellingShingle Piceatannol
Apoptosis
microRNA-181-a
Melanoma cells
Du,Maotao
Zhang,Zhong
Gao,Tao
Piceatannol induced apoptosis through up-regulation of microRNA-181a in melanoma cells
description Abstract Background Melanoma took top position among the lethal cancers and, despite there have been some great attempts made to increase the natural life of patients with metastatic disease, long-lasting and complete remissions are few. Piceatannol, owns the similar function as resveratrol, has been defined as an anti-cancer agent playing important role in inhibition of proliferation, migration and metastasis in various cancer. Thus, we aim to investigate the anti-cancer effect and mechanisms of piceatannol in melanoma cells. Methods Melanoma cell lines WM266-4 and A2058 were treated either with or without piceatannol. Cell viability and cell apoptosis were assessed by using MTT and Annexin V/PI assay, respectively. Cells were transfected with specific miRNA using Lipfectamine 2000. miRNA bingding ability to 3'-UTR region within specific gene was assed by firefly luciferase analysis. Gene and protein expression was eveluated by qRT-PCR and western blot analysis, respectively. Results Our study showed that piceatannol inhibited WM266-4 and A2058 cells growth and induced apoptosis. Totally, 16 differentially expressed miRNAs were screened out including 8 up-regulated and 8 down-regulated miRNAs. Expression level of miR-181a is significantly higher in piceatannol-treated cells than normal control and is lower in melanoma cancer tissues than its adjacent normal tissues. Bcl-2 is a target gene of miR-181a. Moreover, silencing of miR-181a reverses the decrease of cell viability induced by piceatannol in WM266-4 and A2058 cells. Taken together, present study uncovered the ability of piceatannol to repress melanoma cell growth and clarified the contribution of miR-181a in the anticancer role of piceatannol. Conclusion The present study proposes that piceatannol can be taken into account to be a hopeful anticancer agent for melanoma.
author Du,Maotao
Zhang,Zhong
Gao,Tao
author_facet Du,Maotao
Zhang,Zhong
Gao,Tao
author_sort Du,Maotao
title Piceatannol induced apoptosis through up-regulation of microRNA-181a in melanoma cells
title_short Piceatannol induced apoptosis through up-regulation of microRNA-181a in melanoma cells
title_full Piceatannol induced apoptosis through up-regulation of microRNA-181a in melanoma cells
title_fullStr Piceatannol induced apoptosis through up-regulation of microRNA-181a in melanoma cells
title_full_unstemmed Piceatannol induced apoptosis through up-regulation of microRNA-181a in melanoma cells
title_sort piceatannol induced apoptosis through up-regulation of microrna-181a in melanoma cells
publisher Sociedad de Biología de Chile
publishDate 2017
url http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602017000100226
work_keys_str_mv AT dumaotao piceatannolinducedapoptosisthroughupregulationofmicrorna181ainmelanomacells
AT zhangzhong piceatannolinducedapoptosisthroughupregulationofmicrorna181ainmelanomacells
AT gaotao piceatannolinducedapoptosisthroughupregulationofmicrorna181ainmelanomacells
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