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Abstract：
The role of lncRNAs in the pathogenesis of cancer, including colorectal cancer (CRC), has repeatedly been demonstrated. However, very few lncRNAs have been well annotated functionally. Our study identified a novel lncRNA upregulated in CRC, NONHSAT136151, which was correlated with clinical progression. In functional assays, NONHSAT136151 significantly enhanced CRC cell proliferation, migration and invasion. Mechanistically, NONHSAT136151 interacted with RNA-binding protein (RBP) QKI (Quaking) to interfere with QKI binding to target mRNAs and regulate their expression. As well, FOXP3 may be causally related to the dysregulation of NONHSAT136151 in CRC cells through its transcriptional activity. In conclusion, our findings identified a novel lncRNA regulated by FOXP3 participates in CRC progression through interacting with QKI, indicating a novel lncRNA-RBP interaction mechanism is involved in CRC pathogenesis.
摘要：
lncRNAs在癌症发病机制中的作用，包括结直肠癌（CRC），一再被证明。然而,很少有lncRNAs在功能上得到了很好的注释。我们的研究发现了一种在CRC中上调的新lncRNA，NONHSAT136151，与临床进展相关。在功能测定中，NONHSAT136151显著增强CRC细胞增殖，移民和入侵。机械上,NONHSAT136151与RNA结合蛋白（RBP）QKI（Quaking）相互作用，以干扰QKI与靶mRNA的结合并调节其表达。同样,FOXP3可能通过其转录活性与CRC细胞中NONHSAT136151的失调有因果关系。总之,我们的发现鉴定了一种由FOXP3调控的新型lncRNA通过与QKI相互作用参与CRC进展，表明新的lncRNA-RBP相互作用机制参与CRC发病机制。
