4-Chloro-7-Nitrobenzofurazan induces ROS-mediated p53 dependent apoptosis in human fibrosarcoma cells
E H T Thulshan Jayathilaka1, Moon-Moo Kim2
1Department of Cosmetics Engineering, Graduate School of Applied Chemistry·Food Engineering, Dong-Eui University, 176 Eomgwang-ro, Jin- gu, Busan, 47340, Republic of Korea.
Molecular Biology Reports
|July 10, 2026
Summary
4-chloro-7-Nitrobenzofurazan (NBD) selectively targets human fibrosarcoma cells by inducing oxidative stress and apoptosis. This redox-targeting strategy shows promise for treating aggressive fibrosarcoma, a cancer with limited therapeutic options.
Area of Science:
- Biochemistry
- Cell Biology
- Oncology
Background:
- Human fibrosarcoma is an aggressive malignancy with poor therapeutic options.
- Targeting prooxidant pathways offers a potential strategy for fibrosarcoma treatment.
Purpose of the Study:
- To evaluate the anti-cancer effects of 4-chloro-7-Nitrobenzofurazan (NBD) on human fibrosarcoma HT-1080 cells.
- To elucidate the molecular mechanisms underlying NBD's anti-cancer activity.
Main Methods:
- Cell viability assessed via MTT assay in HT-1080 and IMR-90 cells.
- Apoptosis and cell cycle analyzed by flow cytometry.
- Intracellular reactive oxygen species (ROS) and signaling pathways (p53/p21) were evaluated using DCFDA, Western blotting, and reporter assays.
Main Results:
- NBD selectively reduced HT-1080 cell viability (IC50=1.83 µM) while sparing normal cells (IC50=34.02 µM).
- NBD induced apoptosis and G0/G1 cell cycle arrest by increasing intracellular ROS and suppressing catalase.
- NBD activated the p53 pathway, leading to caspase-3 activation and apoptosis, which was reversed by antioxidants or p53 knockout.
Conclusions:
- NBD induces selective apoptosis in fibrosarcoma cells through a ROS-dependent p53 pathway.
- NBD demonstrates potential as a novel redox-targeting therapeutic agent for fibrosarcoma.
