LONG NONCODING RNA;
CANCER-CELLS;
MICRORNAS;
INVASION;
CARCINOMA;
D O I:
10.1155/2022/7723425
中图分类号:
Q81 [生物工程学(生物技术)];
Q93 [微生物学];
学科分类号:
071005 ;
0836 ;
090102 ;
100705 ;
摘要:
Background. The purpose of this study was to explore the functions of FOXD2-AS1 and miR-31 in retinoblastoma. Material and Methods. An RT-qPCR assay was applied to calculate the mRNA levels of FOXD2-AS1, miR-31, and PAX9. A dual-luciferase reporter gene assay was employed to verify the connection between FOXD2-AS1, miR-31, and PAX9 expression. Results. FOXD2-AS1 was upregulated, and miR-31 was lowly expressed in retinoblastoma. Low expression of FOXD2-AS1 promoted cell proliferation and migration, and upregulation of FOXD2-AS1 inhibited proliferative and migratory abilities. lncRNA FOXD2-AS1 directly bound to miR-31 and regulated miR-31 expression in SO-RB50 cells. Cell proliferation and migration were inhibited by the miR-31 mimic. miR-31 mediated PAX9 expression via directly binding to PAX9 mRNA. A miR-31 inhibitor partially reversed the effect of FOXD2-AS1 knockdown on the proliferation and migration in SO-RB50 cells. FOXD2-AS1 knockdown reduced PAX9 expression in SO-RB50 cells. PAX9 had negative connection with miR-31, and it had positive relationship with FOXD2-AS1. Conclusion. lncRNA FOXD2-AS1 inhibited cell proliferation and migration via the miRNA-31/PAX9 axis in retinoblastoma.
机构:
Jilin Univ, Dept Orthopaed, China Japan Union Hosp, 126 Xiantai St, Changchun 130033, Jilin, Peoples R ChinaJilin Univ, Dept Orthopaed, China Japan Union Hosp, 126 Xiantai St, Changchun 130033, Jilin, Peoples R China
Wang, Yang
Kong, Daliang
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机构:
Jilin Univ, Dept Orthopaed, China Japan Union Hosp, 126 Xiantai St, Changchun 130033, Jilin, Peoples R ChinaJilin Univ, Dept Orthopaed, China Japan Union Hosp, 126 Xiantai St, Changchun 130033, Jilin, Peoples R China