MiR-520b as a novel molecular target for suppressing stemness phenotype of head-neck cancer by inhibiting CD44

Abstract Cancer stem cells preferentially acquire the specific characteristics of stress tolerance and high mobility, allowing them to progress to a therapy-refractive state. To identify a critical molecule to regulate cancer stemness is indispensable to erratically cure cancer. In this study, we id...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Ya-Ching Lu, Ann-Joy Cheng, Li-Yu Lee, Guo-Rung You, Yan-Liang Li, Hsin-Ying Chen, Joseph T. Chang
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/7955a3e3428748188f5cdcffdeff18f9
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:7955a3e3428748188f5cdcffdeff18f9
record_format	dspace
spelling	oai:doaj.org-article:7955a3e3428748188f5cdcffdeff18f92021-12-02T16:08:01ZMiR-520b as a novel molecular target for suppressing stemness phenotype of head-neck cancer by inhibiting CD4410.1038/s41598-017-02058-82045-2322https://doaj.org/article/7955a3e3428748188f5cdcffdeff18f92017-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-02058-8https://doaj.org/toc/2045-2322Abstract Cancer stem cells preferentially acquire the specific characteristics of stress tolerance and high mobility, allowing them to progress to a therapy-refractive state. To identify a critical molecule to regulate cancer stemness is indispensable to erratically cure cancer. In this study, we identified miR-520b as a novel molecular target to suppress head-neck cancer (HNC) with stemness phenotype. MiR-520b inhibited cellular migration and invasion via the mechanism of epithelial-mesenchymal transition. It also sensitized cells to therapeutic drug and irradiation. Significantly, miR-520b suppressed spheroid cell formation, as well as reduced expressions of multiple stemness regulators (Nestin, Twist, Nanog, Oct4). The CD44 molecule was identified as a direct target of miR-520b, as shown by the reverse correlative expressions, the response to miR-520 modulation, the luciferase reporter assay, and the functional rescue analyses. These cellular results were confirmed by a tumor xenograft mice study. Administration of miR-520b dramatically restrained tumorigenesis and liver colonization. Conversely, miR-520b silencing led to an acceleration of tumor growth. Taken together, our study demonstrated that miR-520b inhibits the malignancy of HNC through regulation of cancer stemness conversion by targeting CD44. MiR-520b may serve as an emerging therapeutic target that may be further developed for the intervention of refractory HNC.Ya-Ching LuAnn-Joy ChengLi-Yu LeeGuo-Rung YouYan-Liang LiHsin-Ying ChenJoseph T. ChangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-14 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ya-Ching Lu Ann-Joy Cheng Li-Yu Lee Guo-Rung You Yan-Liang Li Hsin-Ying Chen Joseph T. Chang MiR-520b as a novel molecular target for suppressing stemness phenotype of head-neck cancer by inhibiting CD44
description	Abstract Cancer stem cells preferentially acquire the specific characteristics of stress tolerance and high mobility, allowing them to progress to a therapy-refractive state. To identify a critical molecule to regulate cancer stemness is indispensable to erratically cure cancer. In this study, we identified miR-520b as a novel molecular target to suppress head-neck cancer (HNC) with stemness phenotype. MiR-520b inhibited cellular migration and invasion via the mechanism of epithelial-mesenchymal transition. It also sensitized cells to therapeutic drug and irradiation. Significantly, miR-520b suppressed spheroid cell formation, as well as reduced expressions of multiple stemness regulators (Nestin, Twist, Nanog, Oct4). The CD44 molecule was identified as a direct target of miR-520b, as shown by the reverse correlative expressions, the response to miR-520 modulation, the luciferase reporter assay, and the functional rescue analyses. These cellular results were confirmed by a tumor xenograft mice study. Administration of miR-520b dramatically restrained tumorigenesis and liver colonization. Conversely, miR-520b silencing led to an acceleration of tumor growth. Taken together, our study demonstrated that miR-520b inhibits the malignancy of HNC through regulation of cancer stemness conversion by targeting CD44. MiR-520b may serve as an emerging therapeutic target that may be further developed for the intervention of refractory HNC.
format	article
author	Ya-Ching Lu Ann-Joy Cheng Li-Yu Lee Guo-Rung You Yan-Liang Li Hsin-Ying Chen Joseph T. Chang
author_facet	Ya-Ching Lu Ann-Joy Cheng Li-Yu Lee Guo-Rung You Yan-Liang Li Hsin-Ying Chen Joseph T. Chang
author_sort	Ya-Ching Lu
title	MiR-520b as a novel molecular target for suppressing stemness phenotype of head-neck cancer by inhibiting CD44
title_short	MiR-520b as a novel molecular target for suppressing stemness phenotype of head-neck cancer by inhibiting CD44
title_full	MiR-520b as a novel molecular target for suppressing stemness phenotype of head-neck cancer by inhibiting CD44
title_fullStr	MiR-520b as a novel molecular target for suppressing stemness phenotype of head-neck cancer by inhibiting CD44
title_full_unstemmed	MiR-520b as a novel molecular target for suppressing stemness phenotype of head-neck cancer by inhibiting CD44
title_sort	mir-520b as a novel molecular target for suppressing stemness phenotype of head-neck cancer by inhibiting cd44
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/7955a3e3428748188f5cdcffdeff18f9
work_keys_str_mv	AT yachinglu mir520basanovelmoleculartargetforsuppressingstemnessphenotypeofheadneckcancerbyinhibitingcd44 AT annjoycheng mir520basanovelmoleculartargetforsuppressingstemnessphenotypeofheadneckcancerbyinhibitingcd44 AT liyulee mir520basanovelmoleculartargetforsuppressingstemnessphenotypeofheadneckcancerbyinhibitingcd44 AT guorungyou mir520basanovelmoleculartargetforsuppressingstemnessphenotypeofheadneckcancerbyinhibitingcd44 AT yanliangli mir520basanovelmoleculartargetforsuppressingstemnessphenotypeofheadneckcancerbyinhibitingcd44 AT hsinyingchen mir520basanovelmoleculartargetforsuppressingstemnessphenotypeofheadneckcancerbyinhibitingcd44 AT josephtchang mir520basanovelmoleculartargetforsuppressingstemnessphenotypeofheadneckcancerbyinhibitingcd44
_version_	1718384664704450560

MiR-520b as a novel molecular target for suppressing stemness phenotype of head-neck cancer by inhibiting CD44

Ejemplares similares