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FEBS Lett. 2013 Aug 2;587(15):2467-73. doi: 10.1016/j.febslet.2013.06.021. Epub 2013 Jun 22.

miR-26a inhibits proliferation and motility in bladder cancer by targeting HMGA1.

Author information

1
Department of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, China.

Abstract

It is increasingly clear that microRNAs play a crucial role in tumorigenesis. Recently, emerging evidence suggested that miR-26a is aberrantly expressed in tumor tissues. In our study, frequent down-regulation of miR-26a was observed in 10 human bladder cancer tissues. Forced expression of miR-26a in the bladder cancer cell line T24 inhibited cell proliferation and impaired cell motility. High mobility group AT-hook 1 (HMGA1), a gene that modulates cell cycle transition and cell motility, was verified as a novel target of miR-26a in bladder cancer. These findings indicate an important role for miR-26a in the molecular etiology of bladder cancer and implicate the potential application of miR-26a in bladder cancer therapy.

KEYWORDS:

Bladder cancer; Cell cycle; HMGA1; High mobility group AT-hook 1; Invasion; MicroRNA; Migration; high mobility group AT-hook 1; miR-26a; miRNA; microRNA

PMID:
23796420
DOI:
10.1016/j.febslet.2013.06.021
[Indexed for MEDLINE]
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