LncRNA C7orf13 facilitates cell proliferation and metastasis in nasopharyngeal carcinoma via targeting miR‐449c/miR‐28‐5p‐FMNL2 axis

• Published in: Precision medical sciences 2024-12, Vol.13 (4), p.204-213
• Main Authors: Xie, Peng, Zhang, Yujie, Shang, Jin, Yu, Hanxu, Du, Mingyu, Shu, Jian, Wei, Qiang, Zhu, Zeyu, He, Xia
• Format: Article
• Language: English
• Subjects: C7orf13; FMNL2; miR‐28‐5p; miR‐449c; nasopharyngeal carcinoma
• ISSN: 2642-2514; 2642-2514
• DOI: 10.1002/prm2.12152

This study was to determine the involvement of long non‐coding RNA C7orf13 in nasopharyngeal carcinoma (NPC) and its underlying mechanism. Real‐time quantitative PCR results indicated that C7orf13 was overexpressed in NPC and associated with malignant features. C7orf13 knockdown significantly suppressed the proliferation, migration and invasion of NPC cells. Furthermore, we found that C7orf13 sequestered miR‐449c and miR‐28‐5p in NPC cells by dual‐luciferase reporter assays and RNA immunoprecipitation analysis. Sequent experiments showed that C7orf13 has a positive relationship with formin‐like 2 (FMNL2) in NPC tissues. Moreover, C7orf13 knockdown weakened FMNL2‐mediated cell invasion and migration. Finally, functional experiments revealed that the positive effect of C7orf13 on cell migration and invasion was mediated by the miR‐449c/miR‐28‐5p‐FMNL2 axis. Generally, our study identifies the biological role of long non‐coding RNA C7orf13 in the malignant process of NPC, which may pave a new way for the diagnosis and treatment of NPC. Long noncoding RNA C7orf13 aggravates formin‐like 2‐mediated cell invasion and migration via crosstalk with miR‐449c and miR‐28‐5p in nasopharyngeal carcinoma.