Abstract
Accumulating researches have proved that long noncoding RNAs (lncRNAs) regulate a variety of cellular processes during cancer progression. However, the detailed function of most lncRNAs in colorectal cancer (CRC) remains mostly unknown. This study was aimed at exploring the specific role of lncRNA EGOT in CRC. Data from this study revealed that EGOT expression was obviously upregulated in CRC tissues and cell lines, and high EGOT expression indicated poor overall survival of CRC patients. Besides, functional assays proved that EGOT knockdown inhibited cell proliferation and promoted cell apoptosis in CRC. Then, subsequent molecular mechanism assays uncovered that EGOT could bind with miR-33b-5p and negatively regulate miR-33b-5p expression. Additionally, CROT was a downstream target of miR-33b-5p. Further, rescued-function assays suggested that the suppressive influence of EGOT depletion on CRC progression was reversed by miR-33b-5p inhibition or CROT overexpression. In conclusion, lncRNA EGOT mediates the tumor-facilitating part in CRC via miR-33b-5p/CROT pathway.