Open AccessHsa_circRNA_0001971 contributes to oral squamous cell carcinoma progression via miR‐186‐5p/Fibronectin type III domain containing 3B axis
Author(s) -
Zhang Jiehua,
Peng Youjian,
Jiang Shengjun,
Li Jun
Publication year - 2022
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.24245
Subject(s) - gene silencing , cancer research , fibronectin , microrna , blot , cell , chemistry , cell growth , malignancy , microbiology and biotechnology , biology , pathology , medicine , gene , biochemistry
Background Circular RNAs (circRNAs) are closely associated with the progression of oral squamous cell carcinoma (OSCC). circRNA_0001971 has been proved to accelerate the OSCC development. Here, we aim to identify the new molecular mechanism of hsa_circRNA_0001971 (circRNA_0001971) in OSCC. Methods The levels of circRNA_0001971, miR‐186‐5p, and fibronectin type III domain containing 3B (FNDC3B) in tissues and cells were verified by qRT‐PCR or Western blotting. The interaction between circRNA_0001971, miR‐186‐5p, and FNDC3B was identified by bioinformatics analysis, luciferase assay, and RIP assay. The effect of circRNA_0001971/miR‐186‐5p/FNDC3B axis on OSCC cell proliferation, migration, and invasion by cell functional experiments including CCK8, wound healing, and transwell assays. Results Our study displayed that circRNA_0001971 and FNDC3B were elevated in OSCC, whereas miR‐186‐5p was declined in OSCC. Silencing circRNA_0001971 attenuated the malignancy of OSCC cells by suppressing proliferation, migration, and invasion. In OSCC cells, circRNA_0001971 sponged miR‐186‐5p to enhance FNDC3B. Due to the interaction between circRNA_0001971, miR‐186‐5p, and FNDC3B, FNDC3B overexpression relieved the negative function of silencing circRNA_0001971 in OSCC cells. Conclusion Overall, our study discovered that circRNA_0001971 was a tumor promoter in OSCC progression by targeting miR‐186‐5p/FNDC3B axis.