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Published on: April 6, 2012
microRNA-671-5p reduces tumorigenicity of ovarian cancer via suppressing HDAC5 and HIF-1α expression
Dongxian Peng1, Tingting Wu2, Junxia Wang2
1Department of Obstetrics and Gynecology, Zhujiang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, PR China.
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-1α (HIF-1α).
Methods:
miR-671-5p, HDAC5 and HIF-1α 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-1α 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-1α levels were tested in OC tissues. Up-regulating miR-671-5p or down-regulating HDAC5 or HIF-1α 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-1α expression levels.
Insights
MicroRNA-671-5p (miR-671-5p) suppresses ovarian cancer (OC) growth by inhibiting histone deacetylase 5 (HDAC5) and hypoxia-inducible factor-1α (HIF-1α). Lowering miR-671-5p or increasing HDAC5/HIF-1α promotes OC tumorigenicity.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- microRNA (miR)-based therapeutics are increasingly utilized in cancer treatment.
- Ovarian cancer (OC) remains a significant health concern, necessitating novel therapeutic strategies.
- Understanding the molecular mechanisms underlying OC tumorigenesis is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of miR-671-5p in regulating ovarian cancer (OC) tumorigenicity.
- To elucidate the regulatory relationship between miR-671-5p, histone deacetylase 5 (HDAC5), and hypoxia-inducible factor-1α (HIF-1α) in OC.
- To assess the therapeutic potential of modulating miR-671-5p in OC.
Main Methods:
- Expression analysis of miR-671-5p, HDAC5, and HIF-1α in OC tissues and cell lines.
- In vitro transfection of OC cells (H8910) to manipulate miR-671-5p, HDAC5, and HIF-1α levels.
- Assessment of cell proliferation, migration, invasion, and apoptosis following genetic manipulation.
- In vivo studies using animal models to evaluate the impact of miR-671-5p and HDAC5 on tumor growth.
Main Results:
- Downregulation of miR-671-5p and upregulation of HDAC5 and HIF-1α were observed in OC tissues.
- Modulating miR-671-5p, HDAC5, or HIF-1α significantly affected OC cell proliferation, migration, invasion, and apoptosis.
- HDAC5 levels influenced the effect of miR-671-5p on OC cell growth, and in vivo studies confirmed these findings.
Conclusions:
- miR-671-5p acts as a tumor suppressor in ovarian cancer.
- The tumor-suppressive function of miR-671-5p is mediated through the downregulation of HDAC5 and HIF-1α.
- Targeting the miR-671-5p/HDAC5/HIF-1α axis presents a potential therapeutic strategy for ovarian cancer.
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