Related Experiment Video
Updated: May 22, 2026
Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration
Published on: June 9, 2023
7 Methyl indole ethyl isothiocyanate causes ROS mediated apoptosis and cell cycle arrest in endometrial cancer cells
Katrin Kristjansdottir1, Kyukwang Kim, Joong Sub Choi
1Molecular Therapeutics Laboratory, Program in Women's Oncology, Department of Obstetrics and Gynecology, Women and Infants Hospital of Rhode Island, Alpert Medical School, Brown University, Providence, RI 02905, USA.
Objective:
Chemotherapy options for advanced endometrial cancer are limited and newer therapeutic agents are urgently needed. This study describes the therapeutic potential of 7 Methyl-indole ethyl isothiocyanate (7Me-IEITC) in endometrial cancer cell lines.
Methods:
7Me-IEITC was synthesized in our laboratory. The cell viability of 7Me-IEITC treated ECC-1 and KLE endometrial cancer cell was determined by MTS assay. Morphology and apoptosis were further confirmed by DAPI-staining and TUNEL assay. The measurement of reactive oxygen species (ROS), mitochondrial transmembrane depolarization potential (ΔΨm) and cell cycle phase was determined by FACS analysis. Expression of proteins involved in apoptosis, survival and cell-cycle progression was analyzed by Western blotting.
Results:
7Me-IEITC reduced the viability of the ECC-1 and KLE cancer cell-lines (IC(50)~2.5-10 μM) in a dose dependent fashion. 7Me-IEITC treatment caused mitochondrial transmembrane potential reduction, elevated the production of ROS, leading to activation of apoptosis in endometrial cancer KLE and ECC-1 cells. 7Me-IEITC treatment activated Bad, suppressed Bcl2 phosphorylation followed by PARP-1 deactivation and caspase 3 and 7 activation. 7Me-IEITC treatment arrested the progression of KLE cells in S-phase and caused CDC25 and cyclin-D1 downregulation. Pre-treatment with ascorbic acid abrogated 7Me-IEITC induced apoptosis in ECC-1 and KLE cells, suggesting that 7Me-IEITC mediated cytotoxicity is primarily through ROS production.
Conclusion:
7Me-IEITC demonstrated promising cytotoxic effects in endometrial cancer cell line model.
Insights
7 Methyl-indole ethyl isothiocyanate (7Me-IEITC) shows promise as a novel treatment for endometrial cancer by inducing cancer cell death. This compound effectively reduces cancer cell viability and triggers apoptosis through reactive oxygen species generation.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Advanced endometrial cancer presents limited therapeutic options.
- There is an urgent need for novel chemotherapeutic agents.
Purpose of the Study:
- To investigate the therapeutic potential of 7 Methyl-indole ethyl isothiocyanate (7Me-IEITC) in endometrial cancer cell lines.
- To elucidate the mechanisms underlying 7Me-IEITC's cytotoxic effects.
Main Methods:
- 7Me-IEITC was synthesized and its effects on ECC-1 and KLE endometrial cancer cells were evaluated.
- Cell viability was assessed using MTS assay.
- Apoptosis, reactive oxygen species (ROS) production, mitochondrial potential, and cell cycle progression were analyzed via DAPI staining, TUNEL assay, and FACS analysis.
- Protein expression related to apoptosis and cell cycle was examined by Western blotting.
Main Results:
- 7Me-IEITC significantly reduced endometrial cancer cell viability in a dose-dependent manner (IC50 ~2.5-10 μM).
- Treatment induced apoptosis by reducing mitochondrial potential, increasing ROS production, activating caspases (3 and 7), and modulating apoptosis-related proteins (Bad, Bcl2, PARP-1).
- 7Me-IEITC caused S-phase arrest and downregulated cell cycle regulators (CDC25, cyclin-D1). Ascorbic acid pre-treatment reversed these effects, confirming ROS mediation.
Conclusions:
- 7Me-IEITC exhibits significant cytotoxic effects against endometrial cancer cell lines.
- The compound's mechanism involves ROS generation, mitochondrial dysfunction, apoptosis induction, and cell cycle arrest.
- 7Me-IEITC represents a promising candidate for further development as a novel endometrial cancer therapeutic agent.
