Title:Knockdown of miR-135a-5p Promotes Mitophagy by Regulating FoxO1/PINK1/Parkin Signaling in Hepatoma Cells Exposed to Oxidative Stress
Volume: 20
Issue: 3
Author(s): Wang Zhenchang, Zhang Wenfu, Wu Shanshan*Yang Lei*
Affiliation:
- Guangxi International Zhuang Medical Hospital,
Nanning, Guangxi, China
- The First Affiliated Hospital of Guangxi University of Traditional Chinese Medicine, Nanning, Guangxi, China
Keywords:
Hepatoma cells, miR-135a-5p, H2O2, oxidative stress, FoxO1, HCC.
Abstract: Introduction: Excessive oxidative stress is always associated with hepatic disease, including
hepatitis, liver fibrosis, and hepatocellular carcinoma (HCC). Despite this, the intricate molecular
processes driving hepatocyte apoptosis due to oxidative stress remain incompletely comprehended.
Aim: Consequently, we aimed to explore the role of miR-135a-5p in hepatoma cells (HepG2/3B).
Method: The assessment of protein expression was conducted through western blotting. Furthermore,
miR-135a-5p expression was evaluated through RT-qPCR, and apoptosis detection was performed
using a flow cytometry assay.
Result: The findings suggest a connection between miR-135a-5p and mitochondrial-driven apoptosis
through caspase signaling pathways. Furthermore, miR-135a-5p suppression inhibited the apoptotic
response triggered by H2O2, reactive oxygen species (ROS) generation, as well as the decrease
in mitochondrial membrane potential.
Conclusion: Additionally, miR-135a-5p knockdown promoted mitophagy by regulating
FoxO1/PINK1/Parkin signaling via targeting FoxO1. To conclude, our study implied that miR-
135a-5p might function as a probable regulator that protects cells against oxidative stress.