Oncotarget · 2017 · 26 citations · 25 references
Life SciencesMolecular BiologyOncologyGene ExpressionMolecular OncologyNeoplasiaCancer BiomarkersCancer TranscriptomicsNoncoding Rna In CancerRna InterferenceCell Proliferation IndicesCellular Adhesion MoleculesG1 Cell-cycle ArrestNoncoding Rna In ApoptosisWestern Blotting
// Hao Ren 1, 2 , Xiaomin Yang 3 , Yongmei Yang 1 , Xiaoyu Zhang 4 , Rui Zhao 1 , Ran Wei 5 , Xin Zhang 1 , Yi Zhang 1 1 Department of Clinical Laboratory, Qilu Hospital, Shandong University, Jinan, Shandong Province, China 2 Department of Laboratory, Yuhuangding Hospital, Qingdao University Medical College, Yantai, Shandong Province, China 3 Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China 4 Clinical Medicine of Undergraduate, Taishan Medical University, Taian, Shandong Province, China 5 Wakayama 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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