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Knockdown of JARID2 inhibits the proliferation and invasion of ovarian cancer through the PI3K/Akt signaling pathway
- Source :
- Molecular Medicine Reports. 16:3600-3605
- Publication Year :
- 2017
- Publisher :
- Spandidos Publications, 2017.
-
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.
- 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
Subjects
Details
- ISSN :
- 17913004 and 17912997
- Volume :
- 16
- Database :
- OpenAIRE
- Journal :
- Molecular Medicine Reports
- Accession number :
- edsair.doi.dedup.....e84c8dd9a4af7149df633b19b05d5d54