Yang Jin-Lan, Ma Jing-Jing, Qu Tian-Yin, Dai Qing, Leng Jing, Fang Lin, Wu Jie, Li Ya-Jun, Yu Huang-Fei
Department of Oncology, The First People's Hospital of Zunyi (The Third Affiliated Hospital of Zunyi Medical University), Zunyi, 563000, Guizhou Province, China.
Cancer Disease Research Institute, The First People's Hospital of Zunyi (The Third Affiliated Hospital of Zunyi Medical University), 98# Fenghuang Road, Zunyi, 563003, Guizhou Province, China.
Sci Rep. 2025 Mar 22;15(1):9929. doi: 10.1038/s41598-025-94638-2.
Increased evidence reveals that glycolysis is one of the key metabolic hallmarks of cancer cells. However, the roles of lncRNA FTX in energy metabolism and cancer progression remain unclear. In this study we aim to show that lncRNA FTX was significantly upregulated in cancer tissues and serum of CRC patients and CRC cell lines. Function study indicated that it could promote aerobic glycolysis, cell proliferation, migration and invasion in colorectal cancer cells. Further mechanistic studies showed, lncRNA FTX was found to function as a sponge for miR-215-3p, which reduced the ability of miR-215-3p to repress the YAP1 oncoprotein. Additionally, a negative correlation was observed between lncRNA FTX and miR-215-3p expression, and the knockdown of lncRNA FTX or miR-215-3p overexpression yielded opposite effects. In conclusion, this study demonstrates that FTX could directly combine with miR-215-3p as a competitive endogenous RNA, thus promoting the aerobic glycolysis and progression of CRC in vitro and in vivo.
越来越多的证据表明,糖酵解是癌细胞关键的代谢特征之一。然而,长链非编码RNA(lncRNA)FTX在能量代谢和癌症进展中的作用仍不清楚。在本研究中,我们旨在表明lncRNA FTX在结直肠癌(CRC)患者的癌组织和血清以及CRC细胞系中显著上调。功能研究表明,它可促进结肠癌细胞的有氧糖酵解、细胞增殖、迁移和侵袭。进一步的机制研究表明,发现lncRNA FTX可作为miR-215-3p的海绵,降低miR-215-3p抑制YAP1癌蛋白的能力。此外,观察到lncRNA FTX与miR-215-3p表达之间呈负相关,敲低lncRNA FTX或过表达miR-215-3p产生相反的效果。总之,本研究表明FTX可作为竞争性内源性RNA直接与miR-215-3p结合,从而在体外和体内促进CRC的有氧糖酵解和进展。