Borax Suppresses Cellular Viability by Inducing Ferroptosis Signaling Pathway in Endometrial Adenocarcinoma Ishikawa Cells

Betül Keyif; Ceyhan Hacıoğlu

Makale detayları

Borax Suppresses Cellular Viability by Inducing Ferroptosis Signaling Pathway in Endometrial Adenocarcinoma Ishikawa Cells

Yazarlar:

Betül Keyif | Ceyhan Hacıoğlu

Yayıncı:

Akdeniz University

Ana Başlıklar:

Kadın Hastalıkları ve Doğum

Dergi:

Akdeniz Tıp Dergisi Vol.11 Issue 3, pp.477-484

Belge Tipi:

Makale

Yayın Tarihi:

9/2025

Belge Dili:

Türkçe

Document ID (Org No.):

2001357311

pISSN:

2687-2781

Anahtar kelimeler:

Özet:

 Objective: Endometrial cancer is the fourth most frequently diagnosed malignancy and the eighth leading cause of cancer-related mortality among females worldwide. Ferroptosis, a newly identified form of regulated cell death, plays a crucial role in modulating lipid peroxidation through various pathways and is closely associated with both the progression and therapeutic strategies of cancerogenesis. This study aimed to investigate the induction of ferroptosis pathways in borax-treated Ishikawa cells. Material and Methods: To evaluate the effects of borax, assessments of cell viability and proliferation were conducted on Ishikawa cells. Following the determination of boraxs cytotoxic concentrations, morphological analyses were performed alongside the quantification of Fe², malondialdehyde MDA, glutathione GSH, glutathione peroxidase 4 GPx4, and acyl-CoA synthetase long-chain family member 4 ACSL4 levels. Results: The findings revealed that borax reduced Ishikawa cell viability in a concentration- and time-dependent manner. Furthermore, borax significantly inhibited cell proliferation in Ishikawa cells. Inverted microscopic imaging demonstrated that borax induced nuclear abnormalities and reduced the overall cell count. The results further indicated that borax treatment led to a decrease in GSH and GPx4 levels while increasing Fe², MDA, and ACSL4 levels. Conclusion: These findings suggest that borax may serve as a potential anticancer agent for Ishikawa cells by modulating the ferroptosis signaling pathway.

 Objective: Endometrial cancer is the fourth most frequently diagnosed malignancy and the eighth leading cause of cancer-related mortality among females worldwide. Ferroptosis, a newly identified form of regulated cell death, plays a crucial role in modulating lipid peroxidation through various pathways and is closely associated with both the progression and therapeutic strategies of cancerogenesis. This study aimed to investigate the induction of ferroptosis pathways in borax-treated Ishikawa cells. Material and Methods: To evaluate the effects of borax, assessments of cell viability and proliferation were conducted on Ishikawa cells. Following the determination of boraxs cytotoxic concentrations, morphological analyses were performed alongside the quantification of Fe², malondialdehyde MDA, glutathione GSH, glutathione peroxidase 4 GPx4, and acyl-CoA synthetase long-chain family member 4 ACSL4 levels. Results: The findings revealed that borax reduced Ishikawa cell viability in a concentration- and time-dependent manner. Furthermore, borax significantly inhibited cell proliferation in Ishikawa cells. Inverted microscopic imaging demonstrated that borax induced nuclear abnormalities and reduced the overall cell count. The results further indicated that borax treatment led to a decrease in GSH and GPx4 levels while increasing Fe², MDA, and ACSL4 levels. Conclusion: These findings suggest that borax may serve as a potential anticancer agent for Ishikawa cells by modulating the ferroptosis signaling pathway.

 Objective: Endometrial cancer is the fourth most frequently diagnosed malignancy and the eighth leading cause of cancer-related mortality among females worldwide. Ferroptosis, a newly identified form of regulated cell death, plays a crucial role in modulating lipid peroxidation through various pathways and is closely associated with both the progression and therapeutic strategies of cancerogenesis. This study aimed to investigate the induction of ferroptosis pathways in borax-treated Ishikawa cells. Material and Methods: To evaluate the effects of borax, assessments of cell viability and proliferation were conducted on Ishikawa cells. Following the determination of boraxs cytotoxic concentrations, morphological analyses were performed alongside the quantification of Fe², malondialdehyde MDA, glutathione GSH, glutathione peroxidase 4 GPx4, and acyl-CoA synthetase long-chain family member 4 ACSL4 levels. Results: The findings revealed that borax reduced Ishikawa cell viability in a concentration- and time-dependent manner. Furthermore, borax significantly inhibited cell proliferation in Ishikawa cells. Inverted microscopic imaging demonstrated that borax induced nuclear abnormalities and reduced the overall cell count. The results further indicated that borax treatment led to a decrease in GSH and GPx4 levels while increasing Fe², MDA, and ACSL4 levels. Conclusion: These findings suggest that borax may serve as a potential anticancer agent for Ishikawa cells by modulating the ferroptosis signaling pathway.

 Amaç: Endometrial kanser, dünya çapında kadınlarda en sık teşhis edilen dördüncü malignite ve kanserle ilişkili ölümlerin sekizinci önde gelen nedenidir. Yeni tanımlanan bir düzenlenmiş hücre ölümü biçimi olan ferroptozis, çeşitli yollar aracılığıyla lipid peroksidasyonunu düzenlemede önemli bir rol oynar ve kanserogenezin hem ilerlemesi hem de tedavi stratejileriyle yakından ilişkilidir. Bu çalışma, boraksla tedavi edilen Ishikawa hücrelerinde ferroptozis yollarının indüklenmesini araştırmayı amaçlamıştır. Gereç ve Yöntemler: Boraksın etkilerini değerlendirmek için, Ishikawa hücrelerinde hücre canlılığı ve çoğalması değerlendirmeleri yapılmıştır. Boraksın sitotoksik konsantrasyonlarının belirlenmesinin ardından, Fe², malondialdehit MDA, glutatyon GSH, glutatyon peroksidaz 4 GPx4 ve asil-CoA sentetaz uzun zincirli aile üyesi 4 ACSL4 düzeylerinin kantifikasyonuyla birlikte morfolojik analizler gerçekleştirilmiştir. Bulgular: Sonuçlar boraksın Ishikawa hücre canlılığını konsantrasyon ve zamana bağlı bir şekilde azalttığını ortaya koydu. Ayrıca boraks, Ishikawa hücrelerinde hücre çoğalmasını önemli ölçüde engelledi. Ters mikroskopik görüntüleme, boraksın nükleer anormallikleri indüklediğini ve genel hücre sayısını azalttığını gösterdi. Sonuçlar ayrıca boraks tedavisinin GSH ve GPx4 seviyelerinde azalmaya yol açarken Fe², MDA ve ACSL4 seviyelerini artırdığını gösterdi. Sonuç: Bu bulgular boraksın ferroptoz sinyal yolunu düzenleyerek Ishikawa hücreleri için potansiyel bir antikanser ajanı olarak hizmet edebileceğini düşündürmektedir.

Makale detayları

Borax Suppresses Cellular Viability by Inducing Ferroptosis Signaling Pathway in Endometrial Adenocarcinoma Ishikawa Cells

Yazarlar:

Betül Keyif | Ceyhan Hacıoğlu

Yayıncı:

Akdeniz University

Ana Başlıklar:

Kadın Hastalıkları ve Doğum

Dergi:

Akdeniz Tıp Dergisi Vol.11 Issue 3, pp.477-484

Belge Tipi:

Makale

Yayın Tarihi:

9/2025

Belge Dili:

Türkçe

Document ID (Org No.):

2001357311

pISSN:

2687-2781

Borax

Ferroptosis

Endometrial CancerBoraks

Ferroptoz

Endometriyal Kanser

Sayı

Makale detayları

Borax Suppresses Cellular Viability by Inducing Ferroptosis Signaling Pathway in Endometrial Adenocarcinoma Ishikawa Cells

Yazarlar: Betül Keyif | Ceyhan Hacıoğlu

Yayıncı: Akdeniz University

Ana Başlıklar: Kadın Hastalıkları ve Doğum

Dergi: Akdeniz Tıp Dergisi Vol.11 Issue 3, pp.477-484

Belge Tipi: Makale

Yayın Tarihi: 9/2025

Belge Dili: Türkçe

Document ID (Org No.): 2001357311

pISSN: 2687-2781

Borax

Ferroptosis

Endometrial CancerBoraks

Ferroptoz

Endometriyal Kanser

Sayı

Yazarlar:

Betül Keyif | Ceyhan Hacıoğlu

Yayıncı:

Akdeniz University

Ana Başlıklar:

Kadın Hastalıkları ve Doğum

Dergi:

Akdeniz Tıp Dergisi Vol.11 Issue 3, pp.477-484

Belge Tipi:

Makale

Yayın Tarihi:

9/2025

Belge Dili:

Türkçe

Document ID (Org No.):

2001357311

pISSN:

2687-2781