lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-κB/TS Signaling in Colorectal Cancer
Peilong Li, Xin Zhang, Lili Wang, Lutao Du, Yongmei Yang, Tong Liu, Chen Li, Chuanxin Wang
Abstract
(Mol Ther Nucleic Acids. 8, 356–369; September 15, 2017) In the original version of this article, an error in Figure 3F was noted after publication. A version of the right panel of Figure 6K was inadvertently used as the middle panel of Figure 3F. This error occurred during the preparation of figures and went unnoticed during the review process and during preparation of final publication. The revised version of Figure 3 is shown below. This correction does not alter any of the findings or conclusions of the study. The authors regret this error. lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-κB/TS Signaling in Colorectal CancerLi et al.Molecular Therapy - Nucleic AcidsJuly 26, 2017In BriefOne major reason for the failure of advanced colorectal cancer (CRC) treatment is the occurrence of chemoresistance to fluoropyrimidine (FU)-based chemotherapy. Long non-coding RNA HOTAIR has been considered as a pro-oncogene in multiple cancers. However, the precise functional mechanism of HOTAIR in chemoresistance is not well known. In this study, we investigated the biological and clinical role of HOTAIR in 5FU resistance in CRC. Our results showed that HOTAIR negatively regulated miR-218 expression in CRC through an EZH2-targeting miR-218-2 promoter regulatory axis. Full-Text PDF Open Access