LAUSR

Recently, we read a paper “C1QTNF1-AS1 regulates the occurrence and development of hepatocellular carcinoma by regulating miR-221-3p/SOCS3” published in Hepatology International [1]. Authors showed that overexpression of C1QTNF1-AS1 inhibited HCC cell proliferation, migration, and invasion, and promoted apoptosis through the JAK/ STAT signaling pathway. Nonetheless, some problems in this paper attract our attention. In the paper, hepatocellular carcinoma cell lines HepG2 were obtained from American Type Culture Collection and overexpression of C1QTNF1-AS1 inhibited HepG2 tumor growth in vivo (Fig. 6). Nevertheless, based on the evidence in cell bank of Chinese Academy of Science (http://www. cellb ank.org.cn/searc h-detai l.php?id=524) and ATCC (https ://www.atcc.org/produ cts/all/HB-8065.aspx#chara cteri stics ), HepG2 cells cannot form xenografts in nude mice. Furthermore, our lab also confirmed that HepG2 cells do not have tumorigenic ability in mice. Thus, this discrepancy raised our concerns about these results.