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The long non-coding RNA HOTAIR affects the radiosensitivity of pancreatic ductal adenocarcinoma by regulating the expression of Wnt inhibitory factor 1

Overview of attention for article published in Tumor Biology, October 2015
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Title
The long non-coding RNA HOTAIR affects the radiosensitivity of pancreatic ductal adenocarcinoma by regulating the expression of Wnt inhibitory factor 1
Published in
Tumor Biology, October 2015
DOI 10.1007/s13277-015-4234-0
Pubmed ID
Authors

Yanhui Jiang, Zhihua Li, Shangyou Zheng, Huimou Chen, Xiaohui Zhao, Wenchao Gao, Zhuofei Bi, Kaiyun You, Yingxue Wang, Wenzhu Li, Liting Li, Yimin Liu, Rufu Chen

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is seriously resistant to radiotherapy and the mechanism is largely unknown. HOX transcript antisense intergenic RNA (HOTAIR) is overexpressed in PDAC. However, the function of HOTAIR has never been related to the radiosensitivity of PDAC. In this present study, the expression of HOTAIR in the PDAC cell lines and tissues was measured by quantitative real-time PCR (qRT-PCR), and the association between HOTAIR expression levels and X-ray treatment in PDAC cell lines was investigated. Additionally, the influence of HOTAIR knockdown on radiosensitivity, proliferation, and apoptosis of PDAC cells after radiation was evaluated by colony formation assays, Cell Counting Kit-8 (CCK-8) assays, and flow cytometry, respectively. Furthermore, the correlation between HOTAIR and Wnt inhibitory factor 1 (WIF-1) expression in PDAC cell lines and tissues was studied to assess the role of HOTAIR and WIF-1 in the radiosensitivity of PDAC. The results confirmed that HOTAIR expression was significantly increased in the PDAC cell lines and tissues (n = 90) compared with human normal pancreatic ductal epithelial cell line (HPDE) and matched adjacent normal tissues (n = 90). Functionally, HOTAIR knockdown enhanced the radiosensitivity of PDAC cells, reduced the proliferation, and increased the apoptosis of cells after radiation. And HOTAIR silencing increased the expression of WIF-1. Furthermore, the overexpression of WIF-1 revealed that HOTAIR modulated the radiosensitivity of PDAC cells by regulating the expression of WIF-1. These data reveals that HOTAIR can affect the radiosensitivity of PDAC cells partly via regulating the expression of WIF-1, and HOTAIR-WIF-1 axis is a potential target for PDAC radiotherapy.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 37 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 37 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 7 19%
Student > Master 5 14%
Student > Doctoral Student 4 11%
Student > Ph. D. Student 4 11%
Other 3 8%
Other 5 14%
Unknown 9 24%
Readers by discipline Count As %
Medicine and Dentistry 14 38%
Biochemistry, Genetics and Molecular Biology 6 16%
Agricultural and Biological Sciences 2 5%
Unspecified 1 3%
Business, Management and Accounting 1 3%
Other 2 5%
Unknown 11 30%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 21 October 2015.
All research outputs
#20,983,210
of 23,613,071 outputs
Outputs from Tumor Biology
#1,851
of 2,614 outputs
Outputs of similar age
#239,522
of 284,969 outputs
Outputs of similar age from Tumor Biology
#173
of 281 outputs
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