2017年5月29日， 國際學術權威刊物自然出版集團旗下子刊《Nature Cell Biology》雜誌上線上發表了第二軍醫大學醫學遺傳學教研室孫樹漢教授研究組題為“The MBNL3 splicing factor promotes hepatocellular carcinoma by increasing PXN expression through the alternative splicing of lncRNA-PXN-AS1”的研究論文， 論文報導了MBNL3這剪接因數能促進癌症發生， 導致肝細胞癌HCC患者預後不良， 表明了剪接因數和剪接事件可以作為潛在的治療靶點。
文章中， 研究人員發現一種剪接因數：MBNL3能促進癌症發生， 導致肝細胞癌HCC患者預後不良。 研究人員發現敲除MBNL3幾乎完全能消除肝細胞癌腫瘤發生， 這對於肝細胞癌患者來說無疑是一個福音。 肝細胞癌(Hepatocellular carcinoma, HCC)是目前我國致死率居第二位的惡性腫瘤，
MBNL屬於Muscleblind樣蛋白(muscleblind-like proteins， MBNL)， 之前的研究顯示這種蛋白在肌肉和眼睛的發育過程中發揮了重要的功能， 而最新研究通過轉錄組分析表明， MBNL3能誘導lncRNA-PXN-AS1 4號外顯子增加， 這也表明了lncRNA在其中扮演的作用。
這項研究總體來說將剪接因數， 剪接事件與腫瘤發生， 以及lncRNA聯繫在了一起， 表明了剪接因數和剪接事件可以作為潛在的治療靶點。
原文連結：
原文摘要：
Understanding the roles of splicing factors and splicing events during tumorigenesis would open new avenues for targeted therapies. Here we identify an oncofetal splicing factor, MBNL3, which promotes tumorigenesis and indicates poor prognosis of hepatocellular carcinoma patients. MBNL3 knockdown almost completely abolishes hepatocellular carcinoma tumorigenesis. Transcriptomic analysis revealed that MBNL3 induces lncRNA-PXN-AS1 exon 4 inclusion. The transcript lacking exon 4 binds to coding sequences of PXN mRNA, causes dissociation of translation elongation factors from PXN mRNA, and thereby inhibits PXN mRNA translation. In contrast, the transcript containing exon 4 preferentially binds to the 3′ untranslated region of PXN mRNA, protects PXN mRNA from microRNA-24–AGO2 complex-induced degradation, and thereby increases PXN expression. Through inducing exon 4 inclusion, MBNL3 upregulates PXN, which mediates the pro-tumorigenic roles of MBNL3. Collectively, these data demonstrate detailed mechanistic links between an oncofetal splicing factor, a splicing event and tumorigenesis, and establish splicing factors and splicing events as potential therapeutic targets.