Pseudogenes exert potential functions in tumorigenicity and tumour process in human beings. In our previous research on oncogene AKR1B10 in hepatocellular carcinoma (HCC), its pseudogene, AKR1B10P1, was preliminarily noticed being anomalistic transcribed, whereas whether AKR1B10P1 plays any specific function in HCC is poorly understood. By using shRNA transfection and lentiviral infection, we regulated the expression of ARK1B10P1 transcript and the relative targets in two ways. As we discovered, pathological transcription of AKR1B10P1 in HCC cells significantly promotes cell growth and motility either in vitro or in vivo. AKR1B10P1 was correlated with relatively dismal features of HCC. The epithelial‐mesenchymal transition (EMT) was enhanced by up‐regulating AKR1B10P1. And, a potential sequence of AKR1B10P1 transcript was discovered directly interacting with miR‐138. SOX4, a pivotal promotor of EMT, was validated as the down‐streaming target of miR‐138. Mechanistically, degradation of SOX4 mRNA induced by miR‐138 was effectively abrogated by AKR1B10P1. In conclusion, pseudogene AKR1B10P1 exerts stabilizing effect on SOX4 in HCC, associated EMT process, by directly sponging miR‐138, which post‐transcriptionally modulates SOX4’s regulating gene.

中文翻译：

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伪基因AKR1B10P1通过稳定SOX4增强肝细胞癌的致瘤性并调节上皮-间质转化。

假基因在人类的致瘤性和肿瘤过程中发挥潜在的功能。在我们先前对肝细胞癌（HCC）中癌基因AKR1B10的研究中，初步注意到其假基因AKR1B10P1被转录为异常基因，而对AKR1B10P1是否在肝癌中发挥任何特定功能的了解很少。通过使用shRNA转染和慢病毒感染，我们通过两种方式调节ARK1B10P1转录本的表达和相关靶标。正如我们所发现的，AKR1B10P1在HCC细胞中的病理转录在体外或体内均可显着促进细胞生长和运动。AKR1B10P1与肝癌相对较差的特征相关。上调AKR1B10P1可增强上皮-间质转化（EMT）。并且，发现了潜在的AKR1B10P1转录物序列与miR-138直接相互作用。SOX4是EMT的关键推动者，已被证实是miR-138的下游目标。从机理上讲，由AKR1B10P1可以有效地消除miR-138诱导的SOX4 mRNA降解。总之，假基因AKR1B10P1通过直接海绵化miR-138（在转录后调控SOX4的调控基因），在肝癌相关的EMT过程中对SOX4发挥稳定作用。