Surfactin-induced apoptosis through ROS-ERS-Ca2+-ERK pathways in HepG2 cells
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Updated: May 10, 2026
Development and Application of Rapamycin-regulated Tyrosine Phosphatases
Published on: September 6, 2024
Chun-ling Wang1, Chuan Liu, Li-li Niu
1Key Laboratory of Food Nutrition and Safety, Tianjin University of Science & Technology, Ministry of Education, No. 29, 13th Avenue, Tianjin Economy Technological Development Area, Tianjin, 300457, China, wangchunling@tust.edu.cn.
Abstract:
Although surfactin is able to inhibit cancer cell proliferation and to induce cancer cell apoptosis, the molecular mechanism responsible for this process remain elusive. In this study, the signaling network underlying the apoptosis of human hepatoma (HepG2) cells induced by surfactin was investigated. It is found that the reaction oxygen species (ROS) production and intracellular calcium ([Ca(2+)]i) accumulation are both induced HepG2 cells apoptosis. The [Ca(2+)]i exaltation was partly depended on the Ca(2+) release from inositol 1,4,5-trisphosphate (IP3) and ryanodine (Ry) receptors channels, which both triggered endoplasmic reticulum stress (ERS). The results showed that surfactin induced the ROS production and ROS production led to ERS. The occurrence of ERS increased the [Ca(2+)]i level and the processes associated with blocking extracellular signal-regulated kinase (ERK) pathway. According to a comprehensive review of all the evidence, it is concluded that surfactin induces apoptosis of HepG2 cells through a ROS-ERS-Ca(2+) mediated ERK pathway.
Insights
Surfactin triggers cancer cell death by increasing reactive oxygen species (ROS) and calcium levels, activating endoplasmic reticulum stress (ERS), and inhibiting the extracellular signal-regulated kinase (ERK) pathway in human hepatoma cells.
Area of Science:
- Biochemistry
- Cell Biology
- Molecular Oncology
Background:
- Surfactin exhibits anti-cancer properties, inhibiting proliferation and inducing apoptosis.
- The precise molecular mechanisms underlying surfactin-induced apoptosis remain largely unknown.
Purpose of the Study:
- To elucidate the signaling network involved in surfactin-induced apoptosis of human hepatoma (HepG2) cells.
- To investigate the roles of reactive oxygen species (ROS), intracellular calcium ([Ca(2+)]i), and endoplasmic reticulum stress (ERS) in this process.
Main Methods:
- Investigated the effects of surfactin on HepG2 cells.
- Measured ROS production and intracellular calcium ([Ca(2+)]i) levels.
- Assessed the involvement of inositol 1,4,5-trisphosphate (IP3) and ryanodine (Ry) receptors, ERS, and the extracellular signal-regulated kinase (ERK) pathway.
Main Results:
- Surfactin induced ROS production and [Ca(2+)]i accumulation in HepG2 cells.
- ERS was triggered, partly due to Ca(2+) release from IP3 and Ry receptors.
- Surfactin-induced ROS led to ERS, which increased [Ca(2+)]i and inhibited the ERK pathway.
Conclusions:
- Surfactin induces apoptosis in HepG2 cells via a signaling cascade involving ROS, ERS, and calcium.
- The ERK pathway is a key mediator in surfactin-induced cancer cell apoptosis.
