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    • Recent studies suggested that non coding

    2021-10-26

    Recent studies suggested that non-coding RNAs participate in the modulation of Glut1 expression. For instance, the lncRNA NBR2-Glut1 axis was suggested to modulate cancer cell sensitivity to phenformin [37]. In renal carcinoma, miR-1291 is involved in the regulation of Glut1 leptomycin b [38]. Therefore, we evaluated the potential existence of a regular network between lnc-p23154 and Glut1. Here, based on microarray data and bioinformatic prediction, we hypothesized that Glut1 was a putative target gene of miR-378a-3p. The luciferase reporter system and RIP assay showed that miR-378a-3p targeted to the 3ʹUTR of Glut1. Knockdown or overexpression of miR-378a-3p altered Glut1 expression in OSCC cells. Therefore, we concluded that miR-378a-3p suppressed Glut1 expression by targeting its 3ʹUTR directly. We found that lnc-p23154 was mainly localized in the nucleus and contained a complementary sequence within the miR-378a-3p promoter region. It has been established that the molecular mechanism of lncRNAs in cancer varies extensively according to the diverse cellular localization and classifications [39,40]. In the cytoplasm, lncRNAs are involved in post-transcriptional regulation by acting as sponges for miRNAs or proteins [41]. In contrast, lncRNAs enriched in the nucleus regulate gene transcription by remodeling chromatin, i.e., HOTAIR [42] and MALAT1 [43]. Hence, we speculated that lnc-p23154 influences miR-378a-3p transcription. The oligo mimics and decoy sequences, which were designed based on the lnc-p23154/miR-378a-3p binding locus, abolished the effects of miR-378a-3p and Glut1 expression and the metastasis capacity induced by altering lnc-p23154 expression level in OSCC cells. These results indicate that lnc-p23154 targeted to the promoter region of miR-378a-3p and promoted Glut1-mediated metastasis. Similarly, Xue et al. reported that the nucleus-enriched lncRNA DILC inhibited IL-6 transcription by targeting the IL-6 promoter region and contributed to liver cancer stem cell regulation [44].
    Conflicts of interest
    Introduction The facilitated glucose transporter, GLUT1 (SLC2A1), is expressed in a wide variety of cell types and is generally thought to be responsible for basal uptake of glucose, though it responds to changing metabolic conditions as well [1]. Chronic exposure to cell stressors—such as hypoxia, hypoglycemia, and AMP kinase activation—increase GLUT1 protein expression [2], [3], [4]. In addition, this transporter appears to be overexpressed in a number of cancers, especially those driven by KRAS mutations, thereby accelerating glucose uptake [5], [6], [7], [8], [9]. However, there is increasing evidence that the transport activity of GLUT1 can also be regulated acutely in the absence of new protein synthesis. This acute regulation is distinctly different from, and possibly more varied than, the more widely understood transporter, GLUT4, where exposure to insulin in insulin-sensitive tissues and increased contractile activity in myocytes both enhance glucose uptake by stimulating the translocation of GLUT4 transporters from internal stores to the cell surface [10]. The complexity of the acute GLUT1 regulation depends, at least in part, on cell type. For instance, hypoglycemia stimulates GLUT1-mediated glucose uptake in brain capillary endothelial cells via activation of AMP kinase, leading to an increase in the membrane concentrations of GLUT1 [11]. In contrast, hypoglycemia and other cell stressors—such as azide treatment or hyperosmolarity—increased glucose uptake in clone 9 cells, also via activation of AMP kinase, but without a detectable change in concentration of cell surface GLUT1 [12], [13]. The change in activity was attributed to a change in the membrane or lipid environment of the transporter [12], [14], [15], [16], [17]. L929 fibroblast cells, which express GLUT1 at a relatively low concentration, are particularly sensitive to a variety of small molecule activators with different kinetic patterns, suggesting that there may be multiple mechanisms for the acute activation of GLUT1 in this cell line [18], [19], [20].