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HOI-02 induces apoptosis and G2-M arrest in esophageal cancer mediated by ROS
C Zhang1,2,3, K Liu1,2,3,4, K Yao1,4
1Department of Cellular and Molecular Biology, The Hormel Institute, University of Minnesota, Austin, MN, USA.
Abstract:
Reactive oxygen species (ROS) are chemically reactive molecules that perform essential functions in living organisms. Accumulating evidence suggests that many types of cancer cells exhibit elevated levels of ROS. Conversely, generation of ROS has become an effective method to kill cancer cells. (E)-3-hydroxy-3-(4-(4-nitrophenyl)-2-oxobut-3-en-1-yl) indolin-2-one, which is an NO2 group-containing compound designated herein as HOI-02, generated ROS and, in a dose-dependent manner, decreased esophageal cancer cell viability and inhibited anchorage-independent growth, followed by apoptosis and G2-M arrest. Moreover, results of an in vivo study using a patient-derived xenograft mouse model showed that HOI-02 treatment suppressed the growth of esophageal tumors, without affecting the body weight of mice. The expression of Ki-67 was significantly decreased with HOI-02 treatment. In addition, the phosphorylation of c-Jun, and expression of p21, cleaved caspase 3, and DCFH-DA were increased in the HOI-02-treated group compared with the untreated control group. In contrast, treatment of cells with (E)-3-(4-(4-aminophenyl)-2-oxobut-3-en-1-yl)-3-hydroxyindolin-2-one, which is an NH2 group-containing compound designated herein as HOI-11, had no effect. Overall, we identified HOI-02 as an effective NO2 group-containing compound that was an effective therapeutic or preventive agent against esophageal cancer cell growth.
Insights
A novel compound, HOI-02, effectively targets esophageal cancer by generating reactive oxygen species (ROS). This compound reduced tumor growth in mice and induced cancer cell death, offering a potential new therapeutic strategy.
Area of Science:
- Oncology
- Medicinal Chemistry
- Cell Biology
Background:
- Reactive oxygen species (ROS) play dual roles in biological systems, with elevated levels implicated in cancer.
- Targeted ROS generation is a promising strategy for cancer therapy.
Purpose of the Study:
- To investigate the anti-cancer effects of the NO2 group-containing compound HOI-02 on esophageal cancer.
- To evaluate the therapeutic potential of HOI-02 in preclinical esophageal cancer models.
Main Methods:
- In vitro studies assessed HOI-02's effects on esophageal cancer cell viability, growth, apoptosis, and cell cycle progression.
- In vivo efficacy was evaluated using a patient-derived xenograft mouse model of esophageal cancer.
- Molecular markers including Ki-67, c-Jun phosphorylation, p21, cleaved caspase 3, and DCFH-DA were analyzed.
Main Results:
- HOI-02 significantly reduced esophageal cancer cell viability, inhibited anchorage-independent growth, and induced apoptosis and G2-M arrest in a dose-dependent manner.
- In vivo, HOI-02 suppressed tumor growth in xenograft mice without affecting body weight.
- HOI-02 treatment increased apoptosis markers (cleaved caspase 3) and cell cycle inhibitors (p21), and modulated signaling pathways (c-Jun phosphorylation), while decreasing proliferation marker Ki-67.
Conclusions:
- The NO2 group-containing compound HOI-02 demonstrates significant therapeutic potential against esophageal cancer.
- HOI-02 acts, at least in part, by inducing ROS-mediated apoptosis and cell cycle arrest.
- HOI-02 represents a promising candidate for the development of novel esophageal cancer therapeutics.
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