Ni Yin, Li Chunbo, Bo Chen, Zhang Bomiao, Liu Yanlong, Bai Xuefeng, Cui Bingbing, Han Peng
Harbin Medical University Cancer Hospital, Harbin, China.
Biosci Rep. 2020 May 6. doi: 10.1042/BSR20193893.
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.
越来越多的研究证明，长链非编码RNA（lncRNA）在癌症进展过程中调节多种细胞过程。然而，大多数lncRNA在结直肠癌（CRC）中的具体功能仍大多未知。本研究旨在探索lncRNA EGOT在CRC中的具体作用。本研究数据显示，EGOT在CRC组织和细胞系中表达明显上调，且EGOT高表达表明CRC患者总生存期较差。此外，功能实验证明，敲低EGOT可抑制CRC细胞增殖并促进其凋亡。随后，分子机制实验发现，EGOT可与miR-33b-5p结合并负向调节miR-33b-5p表达。此外，CROT是miR-33b-5p的下游靶点。进一步的拯救功能实验表明，抑制miR-33b-5p或过表达CROT可逆转敲低EGOT对CRC进展的抑制作用。总之，lncRNA EGOT通过miR-33b-5p/CROT途径介导CRC的促肿瘤作用。
