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. 2021 Apr 24;23(5):502–514. doi: 10.1016/j.neo.2021.04.001

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© 2021 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 1 — Common binding sites in cooperating genes suggest miR-622 to function as a superior pathway regulator in HCC. (A) In silico screening strategy for identification of further drug resistance and/or stemness related target genes of miR-622 in HCC. Potential novel miR-622 targets were predicted applying miR-target interaction databases ("miRTarBase 2020"; "miRDB"; "TargetScan"; "miRNAMAP 2.0), "string" pathway analysis, and comprehensive literature search applying Medline/PubMed (key terms: "cancer", "stemness", "drug resistance", "liver cancer", "hepatocellular carcinoma" and "microRNA"). (B) Hypothesis of potential regulation of both LIN28A and ZCCHC11 by miR-622 in HCC. Binding of let-7 precursors (pre-let-7) by LIN28A and subsequent oligouridylation by its cooperating partner ZCCHC11 was described to induce depletion of let-7-miRNA [15].