FTO-Mediated lncRNA-FNDRR Axis Demethylation Promotes Cell Proliferation, Invasion, and Migration in Esophageal Squamous Cell Carcinoma

被引:0
|
作者
Liang, Xuyang [1 ,2 ,3 ]
Wang, Libo [2 ]
Wang, Lu [1 ,3 ]
Zhang, Shuxian [1 ,3 ]
Ren, Ling [1 ,3 ]
Li, Shouying [1 ,3 ]
Xu, Jing [1 ,3 ]
Xu, Ping [2 ]
机构
[1] Nanjing Med Univ, Peoples Hosp Lianyungang 1, Lianyungang Clin Coll, Dept Gastroenterol, Lianyungang 222061, Peoples R China
[2] Nanjing Med Univ, Dept Gastroenterol, Shanghai Songjiang Clin Med Coll, Shanghai 201600, Peoples R China
[3] Xuzhou Med Univ, Peoples Hosp Lianyungang 1, Affiliated Lianyungang Hosp, Dept Gastroenterol, Lianyungang 221004, Peoples R China
关键词
Esophageal Squamous Cell Carcinoma; FTO; lncRNA; FNDRR; N6-Methyladenosine; OSTEOSARCOMA CELLS; RNA; CANCER;
D O I
10.1166/jbn.2023.3623
中图分类号
TB3 [工程材料学];
学科分类号
0805 ; 080502 ;
摘要
Esophageal squamous cell carcinoma (ESCC) is characterized by a poor prognosis and has a significant impact on patient survival and quality of life. The role of N6-methyladenosine (m6A) modification in the regulation of long non-coding RNAs (lncRNAs) and messenger RNAs (mRNAs) has been reported in various diseases, including cancer. Although the clinical value of lncRNA-FNDRR in predicting ESCC prognosis is well-established, its molecular mechanism in ESCC remains incompletely understood. Therefore,IP inthis203.8.109.20study,we On:aimed Tue,to 05 investigateSep 2023the 06:29:53involvement of the m6A-lncRNA-FNDRR axis in ESCC progression. Results revealed thaoverxpression of lncRNA-FNDRR exerted inhibitory effects on ESCC cell proliferation, migration, and invasion. Interestingly, knockdown of the demethylase enzyme fat mass and obesityDelivered by Ingen a associated protein (FTO) resulted in similar effects to those achieved by overexpressing lncRNA-FNDRR in ESCC cells. Moreover, we found that FTO had the ability to reverse the m6A modification of lncRNA-FNDRR. Importantly, simultaneous knockdown of FTO and overexpression of lncRNA-FNDRR promoted ESCC cell proliferation and metastasis, suggesting a synergistic effect between these two factors. These results provide valuable insights into the molecular mechanisms underlying ESCC and highlight the significance of m6A modifications in this context. Further investigations on m6A modifications in ESCC are warranted to deepen our understanding of this disease and explore potential therapeutic strategies.
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收藏
页码:1206 / 1215
页数:10
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