摘要
Objective: microRNA (miR)-based therapeutic reference has been established and expanded in the treatment of cancers. For this reason, we explored how miR-671-5p regulated tumorigenicity of ovarian cancer (OC) through regulating histone deacetylase 5 (HDAC5) and hypoxia-inducible factor-1 alpha (HIF-1 alpha). Methods: miR-671-5p, HDAC5 and HIF-1 alpha expression levels were determined in OC clinical tissues. The OC cell line H8910 was screened and transfected with the vectors that altered miR-671-5p, HDAC5 and HIF-1 alpha levels. Finally, the proliferation, migration, invasion and apoptosis of the transfected H8910 cells were determined and the role of miR-671-5p and HDAC5 in vivo tumor growth was further discussed. Results: Low expression miR-671-5p and high expression HDAC5 and HIF-1 alpha levels were tested in OC tissues. Up regulating miR-671-5p or down-regulating HDAC5 or HIF-1 alpha suppressed proliferation, migration, invasion and augmented apoptosis of H8910 cells while silenced miR-671-5p or enhanced HDAC5 caused the opposite consequences. Overexpression of HDAC5 reduced while depletion of HDAC5 enhanced the influence of up-regulated miR-671-5p on OC cell growth. In animal models, suppressing miR-671-5p or promoting HDAC5 encouraged OC tumor growth. Conclusion: A summary delineates that miR-671-5p reduces tumorigenicity of OC via suppressing HDAC5 and HIF-1 alpha expression levels.
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单位南方医科大学