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Long noncoding RNA FER1L4 suppresses cancer cell growth by acting as a competing endogenous RNA and regulating PTEN expression

机译:长非编码RNA FER1L4通过充当竞争性内源RNA并调节PTEN表达来抑制癌细胞的生长

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摘要

Aberrantly expressed long noncoding RNAs (lncRNAs) are associated with various cancers. However, the roles of lncRNAs in the pathogenesis of most cancers are unclear. Here, we report that the lncRNA FER1L4 (fer-1-like family member 4, pseudogene) acts as a competing endogenous RNA (ceRNA) to regulate the expression of PTEN (a well-known tumor suppressor gene) by taking up miR-106a-5p in gastric cancer. We observed that FER1L4 was downregulated in gastric cancer and that its level corresponded with that of PTEN mRNA. Both FER1L4 and PTEN mRNA were targets of miR-106a-5p. Further experiments demonstrated that FER1L4 downregulation liberates miR-106a-5p and decreases the abundances of PTEN mRNA and protein. More importantly, FER1L4 downregulation accelerated cell proliferation by promoting the G0/G1 to S phase transition. We conclude that one mechanism by which lncRNAs function in in tumorigenesis is as ceRNAs for tumor suppressor mRNAs.
机译:异常表达的长非编码RNA(lncRNA)与各种癌症有关。但是,lncRNA在大多数癌症的发病机理中的作用尚不清楚。在这里,我们报道了lncRNA FER1L4(fer-1样家族成员4,假基因)作为竞争性内源RNA(ceRNA)来通过摄取miR-106a来调节PTEN(一种众所周知的抑癌基因)的表达。 -5p在胃癌中。我们观察到FER1L4在胃癌中被下调,并且其水平与PTEN mRNA相对应。 FER1L4和PTEN mRNA均为miR-106a-5p的靶标。进一步的实验表明,FER1L4下调释放了miR-106a-5p,并降低了PTEN mRNA和蛋白质的丰度。更重要的是,FER1L4下调通过促进G0 / G1到S相的转变来加速细胞增殖。我们得出结论,lncRNA在肿瘤发生中起作用的一种机制是作为肿瘤抑制mRNA的ceRNA。

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