long non-coding rna zeb2-as1 promotes hepatocellular carcinoma progression by regulating the mir-582-5p/foxc1 axis

Objectives: long non-coding rnas (lncrnas) feature prominently in tumors. reportedly, lncrna zinc finger e-box-binding homeobox 2 antisense rna 1 (zeb2-as1) is aberrantly expressed in a variety of tumors. the present study was aimed to explore zeb2-as1 functions and determine mechanism in hepatocellular carcinoma (hcc) progression. materials and methods: in this experimental study, expressions of zeb2-as1, microrna (mir)-582-5p and forkhead box c1 (foxc1) mrna in hcc tissues and cell lines were detected via quantitative reveres transcription polymerase chain reaction (qrt-pcr). after establishing gain- and loss-of-functions models, cell counting kit-8, 5-bromo-2’-deoxyuridine (brdu), transwell assays and flow cytometry analysis were conducted to examine hcc cell multiplication, migration, invasion and apoptosis, respectively. the targeted relationship between mir-582- 5p and zeb2-as1 was verified via dual-luciferase reporter gene assay. western blot was utilized for detecting foxc1 expression in hcc cells after selectively regulating zeb2-as1 and mir-582-5p. results: in hcc tissues and cells, zeb2-as1 expression was increased. high zeb2-as1 expression was related to relatively large tumor volume, increased tumor-node-metastasis (tnm) stage and positive lymph node metastasis of the patients. zeb2-as1 overexpression facilitated hcc cell multiplication, migration, invasion and suppressed apoptosis, while zeb2-as1 knock-down caused the opposite effects. it was also confirmed that zeb2-as1 could competitively bind with mir-582-5p to repress its expression, and indirectly up-regulate foxc1 expression level in hcc cells. conclusion: the current study revealed that zeb2-as1 was over-expressed in hcc tissues and cells. it also upregulated foxc1, through sponging mir-582-5p, to promote hcc progression. this provides new perspectives for elucidating the pathogenesis of hcc.