BMC Cancer (Oct 2018)

Uc.416 + A promotes epithelial-to-mesenchymal transition through miR-153 in renal cell carcinoma

  • Yohei Sekino,
  • Naoya Sakamoto,
  • Keisuke Goto,
  • Ririno Honma,
  • Yoshinori Shigematsu,
  • Thang Pham Quoc,
  • Kazuhiro Sentani,
  • Naohide Oue,
  • Jun Teishima,
  • Fumi Kawakami,
  • Jose A Karam,
  • Kanishka Sircar,
  • Akio Matsubara,
  • Wataru Yasui

DOI
https://doi.org/10.1186/s12885-018-4863-y
Journal volume & issue
Vol. 18, no. 1
pp. 1 – 10

Abstract

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Abstract Background The transcribed ultraconserved regions (T-UCRs) are a novel class of non-coding RNAs that are absolutely conserved across species and are involved in carcinogenesis in some cancers. However, the expression and biological role of T-UCRs in renal cell carcinoma (RCC) remain poorly understood. This study aimed to examine the expression and functional role of Uc.416 + A and analyze the association between Uc.416 + A and epithelial-to-mesenchymal transition in RCC. Methods Expression of Uc.416 + A in 35 RCC tissues, corresponding normal kidney tissues and 13 types of normal tissue samples was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). We performed a cell growth and migration assay in RCC cell line 786-O transfected with negative control and siRNA for Uc.416 + A. We evaluated the relation between Uc.416 + A and miR-153, which has a complimentary site of Uc.416 + A. Results qRT-PCR analysis revealed that the expression of Uc.416 + A was higher in RCC tissues than that in corresponding normal kidney tissues. Inhibition of Uc.416 + A reduced cell growth and cell migration activity. There was an inverse correlation between Uc.416 + A and miR-153. Western blot analysis showed Uc.416 + A modulated E-cadherin, vimentin and snail. The expression of Uc.416 + A was positively associated with the expression of SNAI1, VIM and inversely associated with the expression of CDH1. Conclusions The expression of Uc.416 + A was upregulated in RCC and especially in RCC tissues with sarcomatoid change. Uc.416 + A promoted epithelial-to-mesenchymal transition through miR-153. These results suggest that Uc.416 + A may be a promising therapeutic target.

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