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OBJECTIVE The study aimed at elucidating the role of FOXD2-AS1 in facilitating the malignant progression of hepatocellular carcinoma (HCC) by regulating TWIST1. PATIENTS AND METHODS Relative levels of FOXD2-AS1 and TWIST1 in HCC tissues classified by tumor size and tumor node metastasis (TNM) staging were detected by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). The Kaplan-Meier method was applied to assess the prognostic potential of FOXD2-AS1 in HCC patients, followed by survival rate comparison using a log-rank test. After the knockdown of FOXD2-AS1 in HepG2 cells, the viability and migratory abilities were examined by Cell Counting Kit-8 (CCK-8) and transwell assay, respectively. The subcellular distribution of FOXD2-AS1 was detected. Finally, the involvement of TWIST1 in the regulation of HCC cell functions influenced by FOXD2-AS1 was explored. RESULTS FOXD2-AS1 was upregulated in HCC tissues, especially large tumor size or stage III-IV cases. High levels of FOXD2-AS1 predicted poor prognosis in HCC patients. FOXD2-AS1 was mainly distributed in the nucleus, and knockdown of FOXD2-AS1 weakened proliferative and migratory abilities in HepG2 cells. TWIST1 was upregulated in HCC tissues, which was positively correlated to FOXD2-AS1 level. The overexpression of TWIST1 could reverse the inhibited proliferative and migratory abilities in HepG2 cells with FOXD2-AS1 knockdown. CONCLUSIONS FOXD2-AS1 facilitates the progression of HCC by upregulating TWIST1.