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EF24 induces ferroptosis in osteosarcoma cells through HMOX1
Haiyingjie Lin1, Xiaoting Chen2, Chengyong Zhang2
1Department of Orthopedic, The Third Affiliated Hospital of Southern Medical University, No. 183 Zhongshan Dadao West, 510630, Guangzhou, China.
Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|January 16, 2021
Summary
EF24 induces ferroptosis in osteosarcoma cells by upregulating HMOX1, suppressing GPX4, and increasing oxidative stress. This suggests EF24 is a potential treatment for HMOX1-positive osteosarcoma.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- EF24, a curcumin analogue, is an anti-tumor agent.
- Its role in osteosarcoma ferroptosis is unknown.
Purpose of the Study:
- Investigate EF24's effect on osteosarcoma ferroptosis.
- Elucidate the underlying molecular mechanisms.
Main Methods:
- RNA sequencing, cell counting kit-8 assay, flow cytometry, real-time PCR, western blot.
- Assays for malondialdehyde (MDA), reactive oxygen species (ROS), and ferric ion levels.
Main Results:
- EF24 induced osteosarcoma cell death, reversed by ferrostatin-1.
- EF24 increased MDA, ROS, and iron levels, attenuated by ferrostatin-1.
- EF24 upregulated HMOX1, suppressed GPX4, and facilitated ferroptosis.
Conclusions:
- EF24 induces ferroptosis via HMOX1 upregulation and GPX4 suppression.
- EF24 increases MDA, ROS, and iron levels, indicating oxidative stress.
- EF24 is a potential therapeutic agent for HMOX1-positive osteosarcoma.
