1. Knockdown of JARID2 inhibits the proliferation and invasion of ovarian cancer through the PI3K/Akt signaling pathway
- Author
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Guangquan Liu, Huiling Li, Pengfei Xu, Jian Cao, and Suping Han
- Subjects
0301 basic medicine ,Cancer Research ,Epithelial-Mesenchymal Transition ,Biology ,Biochemistry ,Metastasis ,Phosphatidylinositol 3-Kinases ,03 medical and health sciences ,0302 clinical medicine ,Cell Line, Tumor ,Genetics ,medicine ,Humans ,Neoplasm Invasiveness ,Molecular Biology ,Protein kinase B ,PI3K/AKT/mTOR pathway ,Cell Proliferation ,Ovarian Neoplasms ,Oncogene ,Akt/PKB signaling pathway ,Polycomb Repressive Complex 2 ,Cancer ,medicine.disease ,Cell biology ,030104 developmental biology ,Oncology ,Gene Knockdown Techniques ,030220 oncology & carcinogenesis ,Molecular Medicine ,Female ,Signal transduction ,Ovarian cancer ,Proto-Oncogene Proteins c-akt ,Signal Transduction - Abstract
Protein Jumonji (JARID2), a member of the family of JmjC domain-containing proteins, has been reported to serve an important role in tumor growth and metastasis. However, the expression pattern and role of JARID2 in ovarian cancer remains unclear. Therefore, in the present study, the role of JARID2 in ovarian cancer was investigated, as well as the underlying mechanisms. The results of the present study demonstrated that the expression of JARID2 is upregulated in human ovarian cancer cell lines. Furthermore, downregulation of JARID2 significantly suppressed proliferation, migration, invasion and epithelial‑mesenchymal transition in human ovarian cancer cells. Mechanistically, downregulation of JARID2 decreased the protein expression levels of phosphorylated phosphoinositide 3‑kinase (PI3K) and protein kinase B (Akt) in ovarian cancer cells. In conclusion the observations suggested that knockdown of JARID2 inhibited proliferation, migration and invasion in vitro through the inactivation of the PI3K/Akt signaling pathway. Therefore, JARID2 may represent a potential therapeutic target for the treatment of ovarian cancer.
- Published
- 2017