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  • br A set of experiments suggested


    A set of experiments suggested that H19 inhibited apoptosis and promoted the proliferation of GC Talaporfin (Yan et al., 2017). Interestingly, lncRNA H19 is capable of generating miR-675, which is responsible for the regulation of H19 function and differentially expressed in many human tumors (Yan et al., 2017; Cai and Cullen, 2007; Liu et al., 2016). It has been reported that the expression levels of H19 and miR-675 were significantly increased in GC tissues (Yan et al., 2017; Liu et al., 2016; Li et al., 2014). In vitro studies have shown that the H19/miR-675 axis could affect the expression of miR-675-target genes involved in the pathways related to the GC pathogenesis. In this regard, it has been demonstrated that the miR-675 modulates human GC cell proliferation and invasion by targeting tumor suppressor RUNX1 (Liu et al., 2016; Zhuang et al., 2014). Moreover, H19 and its derived miR-675 could inhibit caspase signaling pathway by targeting Fas associated via death domain (FADD) (Yan et al., 2017).
    It has been suggested that lncRNAs that share the same miRNA re-sponse elements (MREs) with mRNA, could impact the expression of each other by competing for miRNA binding. Indeed, lncRNAs can act as endogenous sponges for miRNAs and indirectly regulate gene ex-pression (Hao et al., 2017; Xia et al., 2014). Zhou et al. reported that H19 and miR-141 could compete with each other and affect their tar-gets in GC cells (Zhou et al., 2015a). miR-141 could act as a tumor suppressor in human GC by targeting signal transducer and activator of transcription 4 (STAT4) (Zhou et al., 2014). In addition, miR-141 could inhibit cell proliferation and induce apoptosis in GC cells through binding to 3′-UTR region of the MACC1 gene (Li et al., 2018). This miRNA also inhibits GC proliferation by interacting with MEG3 and down-regulating E2F3 expression (Zhou et al., 2015b).
    We also found that MEG3 expression was down-regulated in GC subjects and low expression of that is correlated with lymph-node metastasis. Deregulated levels of MEG3 could be related to the GC pa-thogenesis and suggested the possibility of using for cancer diagnosis, however, to the best of our knowledge, there are no reports on the investigation of MEG3 lncRNA plasma levels in GC patients. Nonetheless, there is evidence that MEG3 decreased in GC tissues compared with adjacent normal tissues (Sun et al., 2014; Dan et al., 2018). MEG3 can regulate cell cycle progression via control of the protein P53 expression at posttranscriptional level in the development of GC (Sun et al., 2014; Dan et al., 2018). Moreover, Sun et al. reported that MEG3 expression level is correlated with TNM stages and tumor size and patients with low levels of this lncRNA had a relatively poor
    prognosis (Sun et al., 2014). Finally, recent evidence has revealed an interaction between MEG3 and some miRNAs in GC. Amazingly, it has been shown that MEG3 functioned as a “molecular sponge” for miR-181a, miR-148a and miR-141 and thereby modulates the inhibitory effects of these miRNAs on the expression of target genes involved in GC-related pathways (Peng et al., 2015; Yan et al., 2014; Zhou et al., 2015b).
    It has been reported that miR-148a-3p regulates MEG3 in GC by targeting DNA methyltransferase 1 and thereby suppress gastric tu-morigenesis (Yan et al., 2014). miR-148a could also suppress cell in-vasion and migration in GC by regulating DNMT1 expression (Shi et al., 2018). Interestingly, the higher level of H19 which sponged out the low level expressed miR-148a, leading to the overexpression of its target 
    mRNA including DNMT1 and KLF4 (Arun et al., 2018). In this study, we did not observe a significant difference for miR-148a-3p and miR-181a-5p expression levels between controls and GC groups. However, the results revealed that miR-148a-3p levels were markedly increased in newly diagnosed cases of GC compared with GC. Furthermore, GC pa-tients with advanced stages had a lower level of miR-148a-3p than early stages. Consistent with our results, it has been reported that circulating expression of miR-148a was down-regulated in the GC patients (Juzėnas et al., 2015; Qiu et al., 2016). Furthermore, the expression level of this miRNA is associated with tumor size, TNM stage and lymph node metastasis, progression and GC prognosis (Shi et al., 2018; Chen et al., 2010).