Hepatocellular carcinoma (HCC) remains a huge threat to human health even though the diagnosis and treatment strategies have improved rapidly in the past few decades. Increasing evidence has illustrated the critical role noncoding RNA and their regulatory network play in the pathology of HCC. Here, we identified a novel long noncoding RNA, RP5-1120P11.3, that is ectopically expressed in HCC. Further characterization of RP5-1120P11.3 revealed that it promoted proliferation and invasion of HCC cells while inhibiting apoptosis. Importantly, our data revealed that miR-196b-5p interacted with and was regulated by RP5-1120P11.3 via a sponging mechanism. Inhibition of miR-196b-5p attenuated the phenotypes resulting from RP5-1120P11.3 inhibition. Moreover, our data showed that miR-196b-5p inhibited the expression of WIPF2 in HCC, illustrating a regulatory axis of RP5-1120P11.3-miR-196b-5p-WIPF2 that facilitated the progression of HCC. In addition, our data showed that RP5-1120P11.3 contributed to xenograft generation in vivo by regulating miR-196b-5p and WIPF2. These findings suggested that the RP5-1120P11.3-miR-196b-5p-WIPF2 axis is a potential target for treatment of HCC.

中文翻译：

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RP5-1120P11.3通过miR-196b-5p-WIPF2轴促进肝细胞癌的发展。

肝细胞癌（HCC）仍然对人类健康构成巨大威胁，尽管在过去几十年中诊断和治疗策略已得到快速改善。越来越多的证据表明，非编码RNA及其调控网络在HCC病理中起着关键作用。在这里，我们确定了一个新的长非编码RNA，RP5-1120P11.3，在HCC中异位表达。RP5-1120P11.3的进一步表征表明，它在抑制凋亡的同时促进了HCC细胞的增殖和侵袭。重要的是，我们的数据显示miR-196b-5p通过海绵化机制与RP5-1120P11.3相互作用并受其调节。miR-196b-5p的抑制作用减弱了RP5-1120P11.3抑制作用产生的表型。此外，我们的数据显示，miR-196b-5p抑制了HCC中WIPF2的表达，说明了促进肝癌进展的RP5-1120P11.3-miR-196b-5p-WIPF2的调控轴。另外，我们的数据表明，RP5-1120P11.3通过调节miR-196b-5p和WIPF2促进了体内异种移植的产生。这些发现表明，RP5-1120P11.3-miR-196b-5p-WIPF2轴是治疗HCC的潜在靶标。