OBJECTIVE: To investigate the possible role of HOTTIP in the pathogenesis of endometrial cancer (EC) and its underlying mechanism.
PATIENTS AND METHODS: 76 EC tissues and 76 adjacent normal tissues were collected in this study. HOTTIP expression was detected by qRT-PCR (quantitative Real-Time Polymerase Chain Reaction), and its relationship with clinical prognosis of EC patients was then analyzed. The effect of in vitro HOTTIP on proliferation, cell cycle, apoptosis, colony formation, and migration was examined, respectively. Furthermore, the impact of HOTTIP on PI3K/AKT pathway was explored.
RESULTS: HOTTIP was remarkably overexpressed in EC patients. The survival rate of EC patients with high expression of HOTTIP was lower than that of patients with low expression, whereas the pathological grade and tumor size in high expression group were markedly higher than those of low expression group. After upregulation of HOTTIP by lentivirus transfection, the proliferation, colony formation, and migration of EC cells showed a remarkable increase, whereas cell apoptosis was remarkably inhibited. In addition, high expression of HOTTIP promoted the EC development by activating PI3K/AKT pathway.
CONCLUSIONS: Overexpressed HOTTIP promotes the development of endometrial cancer via activating PI3K/AKT pathway.Free PDF Download
To cite this article
Q. Guan, Q. Zhang, C. Zhang, Q. Liu, Q.-L. Ren
HOTTIP regulates progression of endometrial cancer via activating PI3K/AKT pathway
Eur Rev Med Pharmacol Sci
Vol. 22 - N. 12