Molecular Genetics & Genomic Medicine (May 2022)

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

  • Shuai Pei,
  • Chengxian Ma,
  • Jie Chen,
  • Xinyu Hu,
  • Mingyu Du,
  • Tian Xu,
  • Mengna Zhan,
  • Ke Xue,
  • Yufeng Zhang,
  • Li Yin,
  • Xia He

DOI
https://doi.org/10.1002/mgg3.1914
Journal volume & issue
Vol. 10, no. 5
pp. n/a – n/a

Abstract

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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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