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MiR-520b as a novel molecular target for suppressing stemness phenotype of head-neck cancer by inhibiting CD44.
Lu, Ya-Ching; Cheng, Ann-Joy; Lee, Li-Yu; You, Guo-Rung; Li, Yan-Liang; Chen, Hsin-Ying; Chang, Joseph T.
Afiliação
  • Lu YC; Department of Medical Biotechnology and Lab Science, College of Medicine, Chang Gung University, Taoyuan, 333, Taiwan.
  • Cheng AJ; Department of Medical Biotechnology and Lab Science, College of Medicine, Chang Gung University, Taoyuan, 333, Taiwan.
  • Lee LY; Department of Radiation Oncology, Chang Gung Memorial Hospital - Linko, Taoyuan, 333, Taiwan.
  • You GR; Department of Pathology, Chang Gung Memorial Hospital - Linko, Taoyuan, 333, Taiwan.
  • Li YL; Department of Medical Biotechnology and Lab Science, College of Medicine, Chang Gung University, Taoyuan, 333, Taiwan.
  • Chen HY; Department of Medical Biotechnology and Lab Science, College of Medicine, Chang Gung University, Taoyuan, 333, Taiwan.
  • Chang JT; Department of Medical Biotechnology and Lab Science, College of Medicine, Chang Gung University, Taoyuan, 333, Taiwan.
Sci Rep ; 7(1): 2042, 2017 05 17.
Article em En | MEDLINE | ID: mdl-28515423
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.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Células-Tronco Neoplásicas / Regulação Neoplásica da Expressão Gênica / Receptores de Hialuronatos / MicroRNAs / Interferência de RNA / Neoplasias de Cabeça e Pescoço Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Ano de publicação: 2017 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Células-Tronco Neoplásicas / Regulação Neoplásica da Expressão Gênica / Receptores de Hialuronatos / MicroRNAs / Interferência de RNA / Neoplasias de Cabeça e Pescoço Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Ano de publicação: 2017 Tipo de documento: Article