The oncogenic role of ST8SIA6-AS1 in different cancers was reported, including hepatocellular carcinoma (HCC). However, the underlying mechanism has not been completely explored. Real time quantitative PCR analysis was conducted to assess the ST8SIA6-AS1, miR-651-5p and TM4SF4 expression in HCC tissues and cells. Cell counting kit-8 and wound-healing migration assays were adopted to evaluate the HCC cell proliferation and migration, respectively. The expression of apoptosis-related proteins (Bax and Bcl-2) in human colorectal cancer cells (HCC) was determined by western blotting. In addition to bioinformatics analysis, RNA immunoprecipitation studies and luciferase reporter assays were undertaken to investigate the direct target relationship among ST8SIA6-AS1 and miR-651-5p or TM4SF4. Highly expressed ST8SIA6-AS1 and TM4SF4 as well as poorly expressed miR-651-5p were detected in HCC tissues and cells. Clinically, miR-651-5p expression in HCC tissues is negatively correlated with ST8SIA6-AS1 or TM4SF4. Cell functional assays demonstrated that ST8SIA6-AS1 silencing resulted in weakened proliferative and migratory capacities in HCC cells in addition to increase Bax expression and reduced Bcl-2 expression. ST8SIA6-AS1 exhibited its oncogenic function by sponging tumor suppressor miR-651-5p, and the anti-oncogenic of miR-651-5p was offset by its TM4SF4. The manipulation of ST8SIA6-AS1/miR-651-5p/TM4SF4 axis-mediated oncogenicity in HCC might shed new light on HCC diagnosis and therapy.

Long non-coding RNAs (lncRNAs) are critical regulators of hepatocellular carcinoma (HCC) carcinogenesis and development. We aimed to identify the function of the lncRNA ASMTL-AS1 during HCC malignancy. The expression of ASMTL-AS1, miR-1343-3p, and LAMC1 (laminin subunit gamma 1) was assessed in HCC tissues and cells. Cell Counting Kit-8 (CCK8) and Transwell migration assays were performed to determine the effect of ASMTL-AS1 on HCC cell proliferation and migration. Cell apoptosis was identified by detecting Bax and Bcl-2 protein expression using Western blotting, and a xenograft assay was performed to investigate tumor growth in vivo . The interplay between miR-1343-3p and ASMTL-AS1 or LAMC1 was verified through luciferase reporter and RNA immunoprecipitation assays. ASMTL-AS1 and LAMC1 were highly expressed in HCC tissues and cells, whereas miR-1343-3p showed low expression. Clinically, miR-1343-3p expression in HCC tissues showed a negative correlation with ASMTL-AS1 or LAMC1 expression. Functional assays demonstrated that ASMTL-AS1 silencing suppressed HCC cell proliferation and migration and increased cell apoptosis. More interestingly, ASMTL-AS1 sponged miR-1343-3p and miR-1343-3p to target the 3ʹ-UTR of LAMC1, thereby interfering with the malignant behavior of HCC cells. In conclusion, ASMTL-AS1 acts as a carcinogen in HCC through competing endogenous RNA (ceRNA) activity in the miR-1343-3p/LAMC1 axis. Our findings demonstrate that regulating ASMTL-AS1/miR-1343-3p/LAMC1-mediated HCC cell malignancy might be an effective method to interfere with HCC progression.