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  • br regions UTR of targeted mRNAs using miRNA response


    regions (3′-UTR) of targeted mRNAs using miRNA response elements (MRE) to exhibit their posttranscriptional regulatory effects [32]. Computational searches performed in circRNAs for miRNAs Artesunate revealed that many circRNAs contain MREs, indicating that cir-cRNAs may act as miRNAs sponge, decreasing the miRNAs levels and releasing the targeted genes of miRNAs indirectly [33,34]. By per-forming a bioinformatics analysis and dual-luciferase reporter assay, we revealed and validated that circFAT1(e2) reduced the miR-548g levels by directly binding to it. To our best knowledge, this is the first report of miR-548g involvement in the progression of GC. We also found that RUNX1 was the targeted gene of miR-548g by bioinformatics analysis and dual-luciferase reporter assay. Additionally, RUNX1 could abolish 
    the oncogenic effect of miR-548g. These results suggested that cir-cFAT1(e2) in the cytoplasm inhibited GC progression by reducing the miR-548g levels and then releasing the targeted gene of miR-548g RUNX1. RUX1, an important tumor suppressor and transcription factor, was reported to inhibit GC progression [35,36], which was consistent with our results.
    In addition, we investigated the functions of circFAT1(e2) in the nucleus by performing the online catRAPID analysis and circRIP assay. The results showed that circFAT1(e2) may directly interact with YBX1 and the tumor suppressive effect of circFAT1(e2) was abolished by YBX1. YBX1, which belongs to the DNA- and RNA-binding protein fa-mily, was demonstrated to be a potential biomarker in GC diagnosis
    [37]. Furthermore, knockdown of the YBX1 gene suppressed cell mi-gration of GC cells in vitro [38], indicating that YBX1 served as an oncogenic agent in GC, which was also consistent with our findings.
    In conclusion, we revealed that circFAT1(e2) acted as a tumor suppressor in GC by reducing the miR-548g levels in the cytoplasm, and subsequently releasing the miR-548g targeted gene RUNX1. Meanwhile, circFAT1(e2) in the nucleus could bind to the YBX1 protein to inhibit GC progression. However, further analyses needed to be combined to obtain a larger number of circRNAs in GC. Moreover, insulin will be necessary to explore the deeper mechanisms of circFAT1(e2) in GC.
    Disclosure of potential conflicts of interest
    The authors declare no potential conflicts of Artesunate interest.
    Conflicts of interest
    The authors have no commercial or other associations that might pose a conflict of interest.
    This work was supported by the National Youthful Science Foundation of China (Nos. 81302145) and the Science and Technology Research Project of the Science and Technology Bureau of Suzhou City (Nos. SYS201330).
    Appendix A. Supplementary data
    J. Sung, H.F. Kung, Lentivirus-mediated RNA interference targeting enhancer of zeste homolog 2 inhibits hepatocellular carcinoma growth through down-regulation of stathmin, Hepatology 46 (2007) 200–208.
    232 Original Research
    A novel classification of residual disease after interval debulking surgery for advanced-stage ovarian cancer to better distinguish oncologic outcome
    Beryl L. Manning-Geist, MD; Katherine Hicks-Courant, MD; Allison A. Gockley, MD; Rachel M. Clark, MD;
    Marcela G. Del Carmen, MD; Whitfield B. Growdon, MD; Neil S. Horowitz, MD; Ross S. Berkowitz, MD; Michael G. Muto, MD; Michael J. Worley Jr, MD
    BACKGROUND: Complete surgical resection affords the best prog-nosis at the time of interval debulking surgery. When complete surgical resection is unachievable, optimal residual disease is considered the next best alternative. Despite contradicting evidence on the survival benefit of interval debulking surgery if macroscopic residual disease remains, the current definition of “optimal” in patients undergoing interval debulking surgery is defined as largest diameter of disease measuring 1.0 cm, independent of the total volume of disease.