{'fraction_non_alphanumeric': 0.03440094899169632, 'fraction_numerical': 0.030249110320284697, 'mean_word_length': 5.271375464684015, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
MicroRNA-591 Functions as a Tumor Suppressor in Hepatocellular Carcinoma by Lowering Drug Resistance through Inhibition of Far-Upstream Element-Binding Protein 2-Mediated Phosphoinositide 3-Kinase/Akt/Mammalian Target of Rapamycin Axis

MicroRNAs, a group of noncoding regulatory RNAs, are involved in oncogenesis, cell survival, and chemosensitivity. First, microarray-based analysis predicted that far-upstream element-binding protein 2 (FBP2) was upregulated in hepatocellular carcinoma (HCC), which may be regulated by miR-591. In this study, we hypothesize an inhibitory role of miR-591 in HCC via regulating FBP2. Next, reverse transcription quantitative polymerase chain reaction found that FBP2 expressed highly and miR-591 expresses poorly in HCC tissues. Then, the negative correlation between miR-591 and mRNA expression of FBP2 was identified by Pearson’s correlation coefficient, and putative miR-591-binding sites on the 3′-untranslated region of FBP2 was validated using a dual-luciferase reporter gene assay. After the expression of miR-591 and FBP2 was altered in the drug-resistant CD133+/CD44+ cells, a series of in vitro and in vivo experiments demonstrated that either miR-591 overexpression or FBP2 silencing inhibited the abilities of sphere formation and colony formation, drug resistance, as well as tumorigenicity. It was further observed that miR-591 could suppress FBP2 expression by blocking the phosphoinositide 3-kinase/Akt/mammalian target of rapamycin axis. Above results highlighted an inhibitory effect of miR-591 on the development of HCC by reducing the drug resistance of HCC stem cells. It revealed miR-591 as a new target in the treatment of HCC.