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FoxO3a is Essential for the Antiproliferative and Apoptogenic Effects of Sunitinib in MDA-MB231 Cell Line
Hesham M Korashy1, Osamah M Belali2, Mushtaq A Ansar2
1Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Kingdom of Saudi Arabia hkorashy@ksu.edu.sa.
Background:
Sunitinib (SUN), a tyrosine kinase inhibitor, is a promising treatment for triple-negative breast cancer (TNBC), the most aggressive and fast-growing type of breast cancer. Yet, the protective effect of SUN against TNBC is poorly investigated and the role of Forkhead box type O (FOXO3a) transcription factor is still unknown.
Materials And Methods:
Cell proliferation was evaluated using the MTT assay. The mRNA and protein expression of apoptotic, oxidative stress and cell cycle genes were determined by real-time polymerase chain reaction (RT-PCR) and western blot analyses, respectively. Percentage of the apoptotic cells were determined by flow cytometry. The role of FOXO3a was knock-downed using siRNA.
Results:
SUN caused suppression of MDA-MB231 cell growth associated with induction of apoptosis, cell cycle arrest, oxidative stress markers and FOXO3a gene. Importantly, silencing of FOXO3a mRNA using siRNA significantly rescued MDA-MB231 cells from SUN-induced cell-proliferative arrest.
Conclusion:
SUN inhibits TNBC MDA-MB231 cell proliferation through activation of FOXO3a expression.
Insights
Sunitinib (SUN) effectively inhibits triple-negative breast cancer (TNBC) cell growth by inducing apoptosis and cell cycle arrest. This effect is mediated by the activation of the FOXO3a transcription factor.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Triple-negative breast cancer (TNBC) is an aggressive subtype with limited treatment options.
- Sunitinib (SUN), a tyrosine kinase inhibitor, shows potential against TNBC, but its mechanisms are not fully understood.
- The role of the FOXO3a transcription factor in SUN's effect on TNBC remains unexplored.
Purpose of the Study:
- To investigate the protective effect of Sunitinib (SUN) against triple-negative breast cancer (TNBC) MDA-MB231 cells.
- To elucidate the role of the FOXO3a transcription factor in SUN-mediated anti-cancer effects.
Main Methods:
- Cell proliferation was assessed using MTT assays.
- Gene and protein expression related to apoptosis, oxidative stress, and cell cycle were analyzed via RT-PCR and Western blot.
- Apoptosis was quantified by flow cytometry, and FOXO3a was silenced using siRNA.
Main Results:
- Sunitinib suppressed MDA-MB231 cell proliferation and induced apoptosis and cell cycle arrest.
- SUN treatment increased the expression of oxidative stress markers and FOXO3a.
- Silencing FOXO3a significantly reversed the anti-proliferative effects of SUN.
Conclusions:
- Sunitinib inhibits TNBC cell proliferation by activating FOXO3a.
- FOXO3a plays a crucial role in mediating the anti-cancer effects of Sunitinib in TNBC.
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