CircFOXM1 acts as a ceRNA to upregulate SMAD2 and promote the progression of nasopharyngeal carcinoma

鼻咽癌 基因敲除 下调和上调 癌症研究 竞争性内源性RNA 免疫印迹 生物 细胞生长 细胞培养 原位杂交 肿瘤科 医学 病理 内科学 基因 基因表达 长非编码RNA 放射治疗 遗传学
作者
Shuai Pei,Chengxian Ma,Jie Chen,Xinyu Hu,Mengnan Du,Tongwen Xu,Mengna Zhan,Ke Xue,Yufeng Zhang,Yin Li,Xia He
出处
期刊:Molecular Genetics & Genomic Medicine [Wiley]
卷期号:10 (5) 被引量:3
标识
DOI:10.1002/mgg3.1914
摘要

Abstract Background In recent years, the development of high‐throughput sequencing technology has promoted the rapid development of circRNA‐related research. Studies have found that circRNA plays a key role in a variety of tumors, but few people study the role of circRNA in nasopharyngeal carcinoma. Under comprehensive treatments, the 5‐year survival rate can reach about 70%, but some patients still have distant metastases or recurrences after treatment. Therefore, it is very important to study the molecular mechanisms of the proliferation and invasion of nasopharyngeal carcinoma. Methods QRT‐PCR was applied to detect the relative expression level of circFOXM1 in NPC and nasopharyngeal epithelial cell lines. We knocked down circFOXM1 and studied the influence of circFOXM1 on NPC cells. Nuclear and cytoplasmic RNA isolation experiments, fluorescence in situ hybridization (FISH), bioinformatics analysis, the dual‐luciferase reporter experiment, Western Blot, and other experiments were conducted to verify the relationships among circFOXM1, miR‐136‐5p, and SMAD2 . We collected clinical NPC samples to prove the effect of circFOXM1 on the prognosis and treatment of NPC. Results In this study, we found that circFOXM1 is highly expressed in nasopharyngeal carcinoma tissue cells compared with adjacent normal tissues and is related to the staging of nasopharyngeal carcinoma. High expression of circFOXM1 indicates a poor prognosis for nasopharyngeal carcinoma. Knockdown of CircFOXM1 inhibited the proliferation and invasion of nasopharyngeal carcinoma cells. Conclusion CircFOXM1 promotes the malignant proliferation of nasopharyngeal carcinoma cells by regulating the miR‐136‐5p‐SMAD2 axis.

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