期刊
CANCER CELL INTERNATIONAL
卷 21, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s12935-021-02189-z
关键词
Pancreatic cancer; MIR99AHG; ELAVL1; miR-3129-5p; NOTCH2
类别
资金
- General Project of Science and Technology Department of Liaoning Province [20170541044]
The study found that MIR99AHG is overexpressed in PCa and its deficiency inhibits proliferation, migration, and invasion of PCa cells. FOXA1 can induce up-regulation of MIR99AHG, which in turn regulates NOTCH2 expression and activates the Notch signaling pathway by modulating miR-3129-5p and ELAVL1.
Background Pancreatic cancer (PCa) is a fatal malignancy with poor prognosis, high recurrence and mortality. Substantial reports have suggested long non-coding RNAs (lncRNAs) are implicated in development of numerous malignant tumors, and PCa is included. However, the correlation between novel lncRNA mir-99a-let-7c cluster host gene (MIR99AHG) and PCa remains elusive and needs to be deeply investigated. Methods In this study, we firstly used RT-qPCR to examine MIR99AHG expression. Functional assays were implemented for determination of the role of MIR99AHG in PCa cells. Mechanism experiments were designed and carried out for exploring the regulatory mechanism involving MIR99AHG. Results MIR99AHG was distinctly overexpressed in PCa cell lines. MIR99AHG deficiency abrogated PCa cell proliferation, migration and invasion. Moreover, MIR99AHG up-regulation was induced by transcription factor forkhead box A1 (FOXA1). Furthermore, MIR99AHG modulated notch receptor 2 (NOTCH2) expression and stimulated Notch signaling pathway through sequestering microRNA-3129-5p (miR-3129-5p) and recruiting ELAV like RNA binding protein 1 (ELAVL1). Conclusions Altogether, the exploration of FOXA1/MIR99AHG/miR-3129-5p/ELAVL1/NOTCH2 axis in the progression of PCa might provide a meaningful revelation for PCa diagnosis and treatment.
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