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Cell Immunol. 2014 May-Jun;289(1-2):91-6. doi: 10.1016/j.cellimm.2014.03.015. Epub 2014 Apr 3.

ANRIL inhibits p15(INK4b) through the TGFβ1 signaling pathway in human esophageal squamous cell carcinoma.

Author information

1
Institute of Oncology, The Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China.
2
School of Clinical Medicine, Jiangsu University, Zhenjiang 212013, China.
3
Institute of Oncology, The Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China. Electronic address: jq1001@ujs.edu.cn.
4
Department of Thoracic Surgery, The Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China.

Abstract

The INK4b-ARF-INK4a gene cluster encodes three tumor suppressors: p15(INK4b), p14(ARF), and p16(INK4a). Antisense non-coding RNA in the INK4 locus (ANRIL) is transcribed in the opposite direction from this gene cluster. Recent studies suggest that ANRIL represses the expression of p15(INK4b), p14(ARF), and p16(INK4a); however, the underlying mechanism is unclear. In this study, the expressions of ANRIL in human esophageal squamous cell carcinoma (ESCC) tissues and matched adjacent non-tumor tissues were examined by quantitative real-time polymerase chain reaction. Compared with matched adjacent non-tumor tissues, the expression levels of ANRIL in ESCC tissues were significantly increased. Furthermore, inhibition of ANRIL was found to increase the expression of p15(INK4b) and transforming growth factor β1 (TGFβ1) and depletion of ANRIL in ESCC cell lines may inhibit cellular proliferation. Thus, our findings suggest a significant role of ANRIL in the occurrence and development of ESCC through TGFβ1 signaling pathways.

KEYWORDS:

Antisense non-coding RNA in the INK4 locus; Esophageal squamous cell carcinoma; Long non-coding RNA; Transforming growth factor β1; p15(INK4b)

PMID:
24747824
DOI:
10.1016/j.cellimm.2014.03.015
[Indexed for MEDLINE]

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