LINC02163 regulates growth and epithelial-to-mesenchymal transition phenotype via miR-593-3p/FOXK1 axis in gastric cancer cells

Recently, long non-coding RNAs (lncRNAs) were involved in promoting gastric cancer (GC) initiation and progression. In the current study, we revealed that the expression level of LINC02163 was elevated in GC cell lines and tissues. Knockdown of LINC02163 inhibited GC cells growth and invasion both <i>in vitro</i> and <i>in vivo</i>. Mechanismly, LINC02163 exerted as a ceRNA and negatively regulated miR-593-3p expression. In addition, FOXK1 was identified as a down-stream target of miR-593-3p. The miR-593-3p/FOXK1 axis mediated LINC02163’s effect on GC. To the best of our knowledge, our findings provided the first evidence that LINC02163 functioned as an oncogene in GC. LINC02163 may be a candidate prognostic biomarker and a target for new therapies in GC patients.

近年来，长链非编码RNA（long non-coding RNAs，lncRNAs）已被证实参与胃癌（gastric cancer，GC）的发生与进展过程。本研究中，我们发现LINC02163在胃癌细胞系及组织中呈高表达水平。敲低LINC02163可在体外及体内抑制胃癌细胞的增殖与侵袭能力。从机制上看，LINC02163作为内源竞争RNA（competing endogenous RNA，ceRNA）发挥功能，负向调控miR-593-3p的表达。此外，FOXK1被鉴定为miR-593-3p的下游靶基因。miR-593-3p/FOXK1轴介导了LINC02163对胃癌的调控作用。据我们所知，本研究首次证实LINC02163在胃癌中发挥致癌基因的功能。LINC02163有望成为胃癌患者潜在的预后生物标志物及新型治疗靶点。