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The long non-coding RNA ENST00000547547 reduces 5-fluorouracil resistance of colorectal cancer cells via competitive binding to microRNA-31
Author(s) -
Jian Li,
Xiaorong Li,
ChaoQun Cen,
Xiaohui Ai,
Changwei Lin,
Gui Hu
Publication year - 2017
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2017.6082
Subject(s) - oncogene , cancer research , colorectal cancer , gene knockdown , microrna , apoptosis , cell cycle , biology , cancer , downregulation and upregulation , cell growth , cell , medicine , gene , genetics
Colorectal cancer (CRC) is one of the most common cancers and the third leading cause of cancer-related deaths due to its rapid progression and poor prognosis. 5-Fluorouracil (5-FU)-based chemotherapies are the standard treatment for locally advanced CRC. However, a considerable percentage of CRCs have inherent or acquired 5-FU resistance, which critically impedes clinical outcomes. In the present study, we reported that the expression level ENST547547 was downregulated in 5-FU-resistant CRC cells in comparison with the parental cells, While rising with the treatment of 5-FU in parental cells. Overexpression of ENST547547 promoted 5-FU-induced cell apoptosis and reduced the chemoresistance of 5-FU in vitro. Moreover, we found that ENST547547 was a target of miR-31, as confirmed by dual-luciferase reporter assay and RNA immunoprecipitation assay. Notably, miR-31 was upregulated in 5-FU-resistant CRC cells, and knockdown of miR-31 increased the chemosensitivity of 5-FU-resistant CRC cells. Furthermore, we demonstrated that ENST547547 reduced the chemoresistance of 5-FU via competitive binding to miR-31 in 5-FU-resistant CRC cell lines. Collectively, our findings revealed that ENST547547 reduced chemoresistance in 5-FU of 5-FU-resistant CRC cells through competitive binding to miR-31 and has the potential to serve as a therapeutic target in CRC patients.

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