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Dioscin inhibits colon cancer cells' growth by reactive oxygen species-mediated mitochondrial dysfunction and p38 and
Shu Li1, Binbin Cheng2, Lixin Hou1
1Department of Gastroenterology, Baoshan Branch, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine.
Abstract:
Dioscin is a natural steroid saponin derived from several plants that shows potent anticancer effects against a variety of cancer cells. Here, we investigated the antitumor effect of dioscin against human colon cancer cells and evaluated the molecular mechanism involved in this process. The cell cytotoxicity was studied by the MTT assay and BrdU incorporation. The proapoptotic mechanism of dioscin was characterized by flow cytometry analysis. A western blot and an immunofluorescence staining were used to investigate how dioscin induces apoptosis in vitro. In our study, dioscin could significantly inhibit the growth of colon cancer cells in a time-dependent and dose-dependent manner. Dioscin induces apoptosis and reactive oxygen species (ROS) generation, promoting the disruption of mitochondrial membrane potential, Bax translocation to the mitochondria, cytochrome C release to cytosol, activations of caspase-9/3, PARP cleavage, and subsequent apoptosis. Dioscin-induced apoptosis was accompanied by sustained phosphorylation of JNK, p38-MAPK. N-acetyl-L-cysteine, a scavenger of ROS, significantly reversed dioscin-induced cell death and activation of JNK and p38. Collectively, the data indicate that the induction of apoptosis by dioscin is mediated through ROS proteins, which are critical upstream signals for JNK/p38-MAPK activation.
Insights
Dioscin, a plant-derived saponin, effectively inhibits human colon cancer cell growth. It triggers apoptosis via reactive oxygen species (ROS) and the JNK/p38-MAPK pathway, offering a potential natural anticancer agent.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Dioscin is a natural steroid saponin with demonstrated anticancer properties.
- Colon cancer remains a significant global health challenge requiring novel therapeutic strategies.
Purpose of the Study:
- To investigate the antitumor effects of dioscin on human colon cancer cells.
- To elucidate the molecular mechanisms underlying dioscin-induced apoptosis.
Main Methods:
- Cytotoxicity assessed using MTT assay and BrdU incorporation.
- Apoptosis induction analyzed via flow cytometry.
- Western blot and immunofluorescence used to study protein expression and localization.
Main Results:
- Dioscin significantly inhibited colon cancer cell growth in a dose- and time-dependent manner.
- Dioscin induced apoptosis through reactive oxygen species (ROS) generation, mitochondrial dysfunction, and caspase activation.
- Apoptosis was linked to JNK and p38-MAPK pathway activation, which was reversed by ROS scavenging.
Conclusions:
- Dioscin exhibits potent antitumor activity against human colon cancer cells.
- The mechanism involves ROS-mediated activation of the JNK/p38-MAPK pathway, leading to apoptosis.
- Dioscin represents a promising natural compound for colon cancer therapy.