Hepatocellular carcinoma (HCC) is one of the most common cancer and leading cause of cancer-related death worldwide. Baicalein, a principle flavonoid, has shown attractive anti-cancer effects on HCC. However, the underlying molecular mechanisms and influencing factors contributing to the anti-cancer effects of baicalein on HCC are still largely unknown. Long noncoding RNAs (lncRNAs) have been revealed to be fascinating therapeutic targets for cancers. The roles of NF-κB Interacting LncRNA (NKILA) are recently explored in several cancers. However, the expressions, clinical significances, roles and action mechanisms of NKILA in the anti-cancer effects of baicalein on HCC are unknown. In this study, we found that NKILA is down-regulated in HCC and reduced expression of NKILA indicts poor survival of HCC patients. Functional assays showed that overexpression of NKILA enhances the roles of baicalein on HCC cell proliferation inhibition, apoptosis induction, and migration inhibition in vitro and tumor growth suppression in vivo. Conversely, knockdown of NKILA suppresses the effects of baicalein. Mechanistically, we found that NKILA inhibits IκBα phosphorylation, NF-κB nuclear translocation, and NF-κB activity. NKILA also enhances the inhibitory effects of baicalein on NF-κB signaling. Furthermore, the effects of NKILA on baicalein-induced NF-κB activity inhibition, cell growth inhibition, apoptosis induction, and migration inhibition are reversed by NF-κB nuclear translocation inhibitor JSH-23. Collectively, our data demonstrated that NKILA enhances the anti-cancer effects of baicalein on HCC in vitro and in vivo via the regulation of NF-κB signaling, and implied that the combination of NKILA and baicalein would be potential therapeutic strategies for HCC.

肝细胞癌（HCC）是全球最常见的癌症之一，也是与癌症相关的死亡的主要原因。黄ical素是一种主要的类黄酮，对肝癌显示出有吸引力的抗癌作用。然而，仍不知道导致黄ical素对HCC具有抗癌作用的潜在分子机制和影响因素。长的非编码RNA（lncRNA）已被证明是迷人的癌症治疗靶标。NF-κB相互作用LncRNA（NKILA）的作用最近在几种癌症中得到了探索。然而，在黄ical素对肝癌的抗癌作用中，NKILA的表达，临床意义，作用和作用机制尚不清楚。在这项研究中，我们发现NKILA在HCC中被下调，而NKILA的表达降低表明HCC患者的生存期较差。体外和体内肿瘤生长抑制。相反，敲除NKILA可抑制黄ical素的作用。从机理上讲，我们发现NKILA抑制IκBα磷酸化，NF-κB核易位和NF-κB活性。NKILA还增强了黄ical素对NF-κB信号传导的抑制作用。此外，NKILA对黄trans素诱导的NF-κB活性抑制，细胞生长抑制，凋亡诱导和迁移抑制的作用被NF-κB核移位抑制剂JSH-23逆转。总体而言，我们的数据表明NKILA在体外和体内均增强了黄ical素对HCC的抗癌作用 通过调节NF-κB信号传导，暗示NKILA和黄ical素的组合将成为HCC的潜在治疗策略。