4.6
CiteScore
2.2
Impact Factor
- ISSN 1674-8301
- CN 32-1810/R
4.6
2.2
| Citation: |
Juan Zhou, Yiran Xu, Luyao Wang, Yu Cong, Ke Huang, Xinxing Pan, Guangquan Liu, Wenqu Li, Chenchen Dai, Pengfei Xu, Xuemei Jia. LncRNA IDH1-AS1 sponges miR-518c-5p to suppress proliferation of epithelial ovarian cancer cell by targeting RMB47[J]. The Journal of Biomedical Research, 2024, 38(1): 51-65. DOI: 10.7555/JBR.37.20230097
|
Long noncoding RNA (lncRNA) IDH1 antisense RNA 1 (IDH1-AS1) is involved in the progression of multiple cancers, but its role in epithelial ovarian cancer (EOC) is unknown. Therefore, we investigated the expression levels of IDH1-AS1 in EOC cells and normal ovarian epithelial cells by quantitative real-time PCR (qPCR). We first evaluated the effects of IDH1-AS1 on the proliferation, migration, and invasion of EOC cells through cell counting kit-8, colony formation, EdU, transwell, wound-healing, and xenograft assays. We then explored the downstream targets of IDH1-AS1 and verified the results by a dual-luciferase reporter, qPCR, rescue experiments, and Western blotting. We found that the expression levels of IDH1-AS1 were lower in EOC cells than in normal ovarian epithelial cells. High IDH1-AS1 expression of EOC patients from the Gene Expression Profiling Interactive Analysis database indicated a favorable prognosis, because IDH1-AS1 inhibited cell proliferation and xenograft tumor growth of EOC. IDH1-AS1 sponged miR-518c-5p whose overexpression promoted EOC cell proliferation. The miR-518c-5p mimic also reversed the proliferation-inhibiting effect induced by IDH1-AS1 overexpression. Furthermore, we found that RNA binding motif protein 47 (RBM47) was the downstream target of miR-518c-5p, that upregulation of RBM47 inhibited EOC cell proliferation, and that RBM47 overexpressing plasmid counteracted the proliferation-promoting effect caused by the IDH1-AS1 knockdown. Taken together, IDH1-AS1 may suppress EOC cell proliferation and tumor growth via the miR-518c-5p/RBM47 axis.
We acknowledge and appreciate our institutional colleagues for their experimental technical support.
CLC number: R73-3, Document code: A
The authors reported no conflict of interests.
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