期刊
CELL DEATH & DISEASE
卷 9, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41419-018-1117-5
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资金
- CUHK One-off Funding for Joint Lab/Research Collaboration for the CUHK-Shandong University Joint Laboratory on Reproductive Genetics [3132970]
- Shandong University for the CUHK-Shandong University Joint Laboratory on Reproductive Genetics [7104639]
- Natural Science Foundation of Anhui Province for young scholars [1708085QH200]
- Anhui Medical University [4501041101]
We have previously reported that microRNA-10 family could disturb normal development of granulosa cells (GC) during follicle formation. In the current study, the effect of miR-10a on granulosa cell tumor (GCT), a subtype of ovarian cancer, was examined. Strong miR-10a signal was detected in tissues from malignant GCT patients. Forced expression of miR-10a significantly promoted cell proliferation, migration, invasion, ovarian hormone production, and repressed anticancer drug-induced apoptosis in vitro. The oncogenic role of miR-10a was further validated in an orthotopic GCT model in vivo. In addition, by using CRISPR-Cas9 system, the aggressive phenotype was repressed in miR-10a knockout cancer GC. By using a heterotopic mice model, the oncogenic role of miR-10a was confirmed in vivo. RNA-seq, FISH, western blot, luciferase reporter assay were used to identified PTEN, a well-known anti-GCT gene, as direct functional target of miR-10a in cancer GC; Akt and Wnt were also found as two associated oncogenic pathways of miR-10a in cancer GC. Taken together, our results demonstrate that the miR-10a could promote GCT development via synergistically regulating PTEN, Akt, and Wnt pathways.
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