Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2017;43(5):1767-1776.
doi: 10.1159/000484063. Epub 2017 Oct 19.

Mir-29b Regulates Oxidative Stress by Targeting SIRT1 in Ovarian Cancer Cells

Meng Hou  1 , Xiaohang Zuo  2 , Chen Li  1 , Yan Zhang  3 , Yue Teng  1
Affiliations
Free article

Mir-29b Regulates Oxidative Stress by Targeting SIRT1 in Ovarian Cancer Cells

Meng Hou et al. Cell Physiol Biochem. 2017.
Free article

Abstract

Background: Metabolic abnormalities are frequently observed in multiple malignancies including epithelial ovarian cancer (EOC), among which imbalance between generation and elimination of reactive oxygen species (ROS) plays a critical role in EOC onset and progression. Here we investigated the role of miR-29b, a well-established tumor-suppressor miRNA in metabolic regulation of EOC cells.

Methods: cell viability and apoptosis in miR-29b inhibited and over-expressed EOC cells were evaluated by CCK8 and Annexin V-FITC/PI assays. Change in miR-29b was detected in EOC cells incubated in H2O2 culture by q-PCR. Relative ROS levels were also detected in different EOC cultures, including modified miR-29b and SIRT1 levels as well as H2O2 incubation. A luciferase reporter assay was employed to detect the direct binding of miR-29b to SIRT1 3' UTR. Changes in cell viability and ROS levels were assessed in SIRT1-knocked down EOC cells.

Results: miR-29b expression correlates with decreased EOC cell viability and increased apoptosis. H2O2 downregulated miR-29b in a time and dose-dependent manner. miR-29b expression negatively correlated with ROS levels, whereas SIRT1 significantly stimulated ROS formation. Luciferase reporter assays confirmed miR-29b downregulation of SIRT1by directly targeting its mRNA 3'-UTR. SIRT1 silencing rescues cell viability of H2O2 treated cells. Also, SIRT1 inhibition blocked cell apoptosis induced by H2O2 as well as reduced intracellular ROS levels.

Conclusion: Together, our findings indicated that the miR-29b/SIRT1 axis has a protective effect against H2O2-induced damage of cell viability and oxidative stress and may provide novel options for miR-29b-based therapeutic approaches for EOC treatment.

Keywords: Micro-RNAs; Ovarian Cancer; ROS (reactive oxygen species); SIRT1 (silent mating type information regulation 2 homolog 1).

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

MeSH terms

LinkOut - more resources