Oncotarget

Research Papers:

LITAF is a potential tumor suppressor in pancreatic cancer

Yuan Zhou, Jing Huang, Xi Yu, Xin Jiang, Yaoyao Shi, Yuanyuan Weng, Yue Kuai, Lizhen Lei, Guoping Ren, Xiaowen Feng, Guoping Zhong, Qingmeng Liu, Hongyang Pan, Xinxia Zhang, Ren Zhou and Caide Lu _

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Oncotarget. 2018; 9:3131-3142. https://doi.org/10.18632/oncotarget.23220

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Abstract

Yuan Zhou1,2,4, Jing Huang1, Xi Yu1, Xin Jiang3, Yaoyao Shi3, Yuanyuan Weng3, Yue Kuai3, Lizhen Lei3, Guoping Ren4, Xiaowen Feng4, Guoping Zhong5, Qingmeng Liu6, Hongyang Pan7, Xinxia Zhang7, Ren Zhou3 and Caide Lu1,2

1Department of Hepatopancreatobiliary Surgery, Ningbo Medical Center Lihuili Eastern Hospital, Ningbo, China

2Medical School of Ningbo University, Ningbo, China

3Department of Pathology and Pathophysiology, Institute of Pathology and Forensic Medicine, Zhejiang University School of Medicine, Hangzhou, China

4The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China

5Division of Pathology, Yinzhou Hospital Affiliated to Medical School of Ningbo University, Ningbo, China

6Division of Pathology, The Second People’s Hospital, Shaoxing, China

7Epitomics (Hangzhou) Inc., Hangzhou, Zhejiang, P.R. China

Correspondence to:

Caide Lu, email: lucaide@nbu.edu.cn

Keywords: lipopolysaccharide-induced tumor necrosis factor-α factor (LITAF); pancreatic cancer; promoter methylation; tumor suppressor gene

Received: April 20, 2016     Accepted: November 15, 2017     Published: December 14, 2017

ABSTRACT

Early diagnosis of pancreatic cancer, one of the most deadly cancers with low survival rates, is difficult, and effective biomarkers are urgently needed. Lipopolysaccharide-induced tumor necrosis factor-α factor (LITAF) has been recently proposed as a potential tumor suppressor gene in several types of cancer. Here, we analyzed the biological function of LITAF in pancreatic cancer. The LITAF gene and protein levels were decreased in pancreatic tumor tissues compared with their paired adjacent non-cancerous tissues. In addition, patients with the lower LITAF protein expression had lower disease-free survival rates. The decreased LITAF expression correlated with LITAF promoter hypermethylation in pancreatic cancer cells and tissues. Moreover, promoter demethylation dose-dependently increased the LITAF transcription. Importantly, LITAF demethylation suppressed proliferation and cell cycle progression, and enhanced apoptosis of pancreatic cancer cells. Together, our results indicate that LITAF functions as a tumor suppressor gene in pancreatic cancer cells, and might serve as a novel biomarker for early diagnosis of pancreatic cancer.


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