Oncotarget

Research Papers:

Upregulation of LncRNA BCYRN1 promotes tumor progression and enhances EpCAM expression in gastric carcinoma

Hao Ren, Xiaomin Yang, Yongmei Yang, Xiaoyu Zhang, Rui Zhao, Ran Wei, Xin Zhang and Yi Zhang _

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Oncotarget. 2018; 9:4851-4861. https://doi.org/10.18632/oncotarget.23585

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Abstract

Hao Ren1,2, Xiaomin Yang3, Yongmei Yang1, Xiaoyu Zhang4, Rui Zhao1, Ran Wei5, Xin Zhang1, Yi Zhang1

1Department of Clinical Laboratory, Qilu Hospital, Shandong University, Jinan, Shandong Province, China

2Department of Laboratory, Yuhuangding Hospital, Qingdao University Medical College, Yantai, Shandong Province, China

3Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China

4Clinical Medicine of Undergraduate, Taishan Medical University, Taian, Shandong Province, China

5Wakayama Medical University, Wakayama, Wakayama, Japan

Correspondence to:

Yi Zhang, email: yizhang@sdu.edu.cn

Keywords: BCYRN1; lncRNA; gastric carcinoma; tumor progression; EpCAM

Received: June 09, 2017     Accepted: December 13, 2017     Published: December 21, 2017

ABSTRACT

Brain cytoplasmic RNA 1 (BCYRN1), along non-coding RNA, plays a critical role in various diseases, including some cancers. However, the expression of BCYRN1 and its roles in gastric carcinoma (GC) still remain unidentified. Thus, this study employed RT-qPCR to detect expression of BCYRN1 in 85 paired GC samples and adjacent normal tissues, and performed in vitro studies to explore effects of BCYRN1 in GC cells on cell proliferation, apoptosis and migration. We found BCYRN1 was significantly upregulated in GC samples, and its expression was positively correlated with advanced TNM stage (p = 0.0012) and tumor size (p = 0.027). Functionally, BCYRN1 knockdown by siRNA could inhibit cell proliferation, induce G1/G0 cell cycle arrest, increase apoptosis and impair migratory ability of AGS cells. Moreover, the results of RT-qPCR and western blotting indicated that knockdown of BCYRN1 notably decreased the expression of epithelial cell adhesion molecules (EpCAM). Otherwise, overexpression of BCYRN1 in GC cells (BGC-823 and SGC-7901) could reverse the effects of BCYRN1 knockdown. Taken together, our data indicate for the first time that BCYRN1 acts as an oncogenic lncRNA in GC progression and may be a potential therapeutic target in GC.


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