FOXP3‐regulated lncRNA NONHSAT136151 promotes colorectal cancer progression by disrupting QKI interaction with target mRNAs

Author:

Huang Handong12ORCID,Liang Xiaoxiang2,Wu Weizheng2,Yuan Tao2,Chen Zhengquan2,Wang Lin2,Wu Zhenyu2,Zhang Tao2,Yang Kai2,Wen Kunming12

Affiliation:

1. Soochow University Medical College Suzhou Jiangsu China

2. Department of General Surgery Affiliated Hospital of Zunyi Medical University Zunyi Guizhou China

Abstract

AbstractThe 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.

Funder

National Natural Science Foundation of China

Publisher

Wiley

Subject

Cell Biology,Molecular Medicine

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