Quinazolinedione Derivatives as Potential Anticancer Agents Through Apoptosis Induction in MCF-7
1
Issued Date
2025-07-01
Resource Type
ISSN
16616596
eISSN
14220067
Scopus ID
2-s2.0-105010327330
Journal Title
International Journal of Molecular Sciences
Volume
26
Issue
13
Rights Holder(s)
SCOPUS
Bibliographic Citation
International Journal of Molecular Sciences Vol.26 No.13 (2025)
Suggested Citation
Limboonreung T., Suansilpong T., Jumjitvi P., Lohawittayanan D., Krobthong S., Charoensutthivarakul S. Quinazolinedione Derivatives as Potential Anticancer Agents Through Apoptosis Induction in MCF-7. International Journal of Molecular Sciences Vol.26 No.13 (2025). doi:10.3390/ijms26136038 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/111278
Title
Quinazolinedione Derivatives as Potential Anticancer Agents Through Apoptosis Induction in MCF-7
Corresponding Author(s)
Other Contributor(s)
Abstract
Breast cancer remains a leading cause of mortality among women worldwide. Surgery, radiation therapy, chemotherapy, and hormone-based treatments are standard therapeutic approaches, but drug resistance and adverse effects necessitate the search for novel anticancer agents. Quinazolinedione derivatives have emerged as potential anticancer compounds due to their cytotoxic and apoptosis-inducing properties. This study aimed to evaluate the apoptotic induction of previously reported quinazolinedione derivatives on MCF-7 breast cancer cells. The cytotoxic effect was assessed using the MTT assay, apoptosis was quantified by Annexin V-PE/7AAD staining and flow cytometry, and apoptosis-related protein expression was analyzed via multiplexed bead-based immunoassays. These findings indicate that two derivatives in the series significantly reduced the cell viability in a dose-dependent manner. Apoptosis was induced primarily through the intrinsic apoptotic pathway as evidenced by the upregulation of caspase-9 and p53 and the downregulation of Bcl-2 and p-Akt. These results highlight quinazolinedione derivatives as promising candidates for breast cancer therapy prompting further investigation into their molecular mechanisms and potential clinical applications.
