Capsaicin Induces Apoptosis in Endometrial Cancer Cells via Endoplasmic Stress and Triggers Antiproliferative Effects

Betül Keyif; Ceyhan Hacıoğlu

Makale detayları

Capsaicin Induces Apoptosis in Endometrial Cancer Cells via Endoplasmic Stress and Triggers Antiproliferative Effects

Yazarlar:

Betül Keyif | Ceyhan Hacıoğlu

Yayıncı:

Kirsehir Ahi Evran University

Ana Başlıklar:

Klinik Kimya

Dergi:

Ahi Evran Tıp Dergisi Vol.9 Issue 2, pp.186-194

Belge Tipi:

Makale

Yayın Tarihi:

8/2025

Belge Dili:

Türkçe

Document ID (Org No.):

2001345471

pISSN:

2619-9203

Anahtar kelimeler:

Özet:

 Purpose: Endometrial cancer is a common gynecological malignancy globally. Endoplasmic reticulum ER stress, characterized by disrupted cellular homeostasis, is implicated in cancer progression. Capsaicin, a bioactive compound with known antiproliferative properties, may act as a therapeutic agent by inducing ER stress in cancer cells. This study explores the mechanisms by which capsaicin triggers ER stress in endometrial cancer cells. Materials and Methods: Ishikawa endometrial cancer cells were treated with capsaicin 0800 μM, and cell viability was asses-sed using the MTT assay. Capsaicin reduced viability in a dose-dependent manner, with an IC50 of 285.2 μM at 24 hours. BrdU assays further confirmed the suppression of proliferation. To evaluate the involvement of ER stress and apoptosis, levels of GRP78, ATF6, CHOP ER stress markers, and cytochrome c and caspase-3 apoptotic markers were measured via ELISA. Results: Capsaicin treatment significantly reduced cell viability and proliferation in a concentration- and timedependent manner. Elevated levels of GRP78, ATF6, and CHOP confirmed the induction of ER stress p0.05. Concurrently, increased cytochrome c and caspase-3 levels indicated the activation of apoptosis. Conclusion: Capsaicin induces ER stress-mediated apoptosis in Ishikawa endometrial cancer cells, suggesting its therapeutic potential in targeting cancer progression. Further in vivo investigations are warranted to confirm its efficacy and underlying mechanisms.

 Purpose: Endometrial cancer is a common gynecological malignancy globally. Endoplasmic reticulum ER stress, characterized by disrupted cellular homeostasis, is implicated in cancer progression. Capsaicin, a bioactive compound with known antiproliferative properties, may act as a therapeutic agent by inducing ER stress in cancer cells. This study explores the mechanisms by which capsaicin triggers ER stress in endometrial cancer cells. Materials and Methods: Ishikawa endometrial cancer cells were treated with capsaicin 0800 μM, and cell viability was asses-sed using the MTT assay. Capsaicin reduced viability in a dose-dependent manner, with an IC50 of 285.2 μM at 24 hours. BrdU assays further confirmed the suppression of proliferation. To evaluate the involvement of ER stress and apoptosis, levels of GRP78, ATF6, CHOP ER stress markers, and cytochrome c and caspase-3 apoptotic markers were measured via ELISA. Results: Capsaicin treatment significantly reduced cell viability and proliferation in a concentration- and timedependent manner. Elevated levels of GRP78, ATF6, and CHOP confirmed the induction of ER stress p0.05. Concurrently, increased cytochrome c and caspase-3 levels indicated the activation of apoptosis. Conclusion: Capsaicin induces ER stress-mediated apoptosis in Ishikawa endometrial cancer cells, suggesting its therapeutic potential in targeting cancer progression. Further in vivo investigations are warranted to confirm its efficacy and underlying mechanisms.

 Purpose: Endometrial cancer is a common gynecological malignancy globally. Endoplasmic reticulum ER stress, characterized by disrupted cellular homeostasis, is implicated in cancer progression. Capsaicin, a bioactive compound with known antiproliferative properties, may act as a therapeutic agent by inducing ER stress in cancer cells. This study explores the mechanisms by which capsaicin triggers ER stress in endometrial cancer cells. Materials and Methods: Ishikawa endometrial cancer cells were treated with capsaicin 0800 μM, and cell viability was asses-sed using the MTT assay. Capsaicin reduced viability in a dose-dependent manner, with an IC50 of 285.2 μM at 24 hours. BrdU assays further confirmed the suppression of proliferation. To evaluate the involvement of ER stress and apoptosis, levels of GRP78, ATF6, CHOP ER stress markers, and cytochrome c and caspase-3 apoptotic markers were measured via ELISA. Results: Capsaicin treatment significantly reduced cell viability and proliferation in a concentration- and timedependent manner. Elevated levels of GRP78, ATF6, and CHOP confirmed the induction of ER stress p0.05. Concurrently, increased cytochrome c and caspase-3 levels indicated the activation of apoptosis. Conclusion: Capsaicin induces ER stress-mediated apoptosis in Ishikawa endometrial cancer cells, suggesting its therapeutic potential in targeting cancer progression. Further in vivo investigations are warranted to confirm its efficacy and underlying mechanisms.

 Amaç: Endometriyal kanser, dünya genelinde yaygın görülen bir jinekolojik malignitedir. Hücresel homeostazın bozulmasıyla tanımlanan endoplazmik retikulum ER stresi, kanserin ilerlemesinde önemli bir rol oynamaktadır. Antiproliferatif özellikleri bilinen biyoaktif bir bileşik olan kapsaisin, kanser hücrelerinde ER stresi oluşturarak potansiyel bir tedavi ajanı olabilir. Bu çalışma, kapsaisinin endometriyal kanser hücrelerinde ER stresini nasıl tetiklediğini araştırmayı amaçlamaktadır. Araçlar ve Yöntem: İshikawa endometriyal kanser hücreleri 0800 μM aralığında kapsaisin ile muamele edildi ve hücre canlılığı MTT testi ile değerlendirildi. Kapsaisin, 24 saatlik uygulamada 285.2 μM IC50 değeri ile doza bağımlı bir şekilde hücre canlılığını azalttı. BrdU testleri de çoğalmanın baskılandığını doğruladı. ER stresi ve apoptozun değerlendirilmesi için GRP78, ATF6, CHOP ER stres belirteçleri ile sitokrom c ve kaspaz-3 apoptoz belirteçleri düzeyleri ELISA yöntemiyle ölçüldü. Bulgular: Kapsaisin, hücre canlılığını ve çoğalmasını konsantrasyon ve zamana bağlı olarak anlamlı biçimde azalttı. GRP78, ATF6 ve CHOP düzeylerindeki artış, ER stresinin indüklendiğini gösterdi p0.05. Aynı zamanda sitokrom c ve kaspaz-3 düzeylerinin artması, apoptozun da aktive olduğunu ortaya koydu. Sonuç: Kapsaisin, İshikawa endometriyal kanser hücrelerinde ER stresi aracılı apoptozu tetikleyerek kanserin ilerlemesini engelleme potansiyeline sahiptir. Ancak, etkinliğini ve mekanizmalarını doğrulamak için in vivo çalışmalara ihtiyaç vardır.

Makale detayları

Capsaicin Induces Apoptosis in Endometrial Cancer Cells via Endoplasmic Stress and Triggers Antiproliferative Effects

Yazarlar:

Betül Keyif | Ceyhan Hacıoğlu

Yayıncı:

Kirsehir Ahi Evran University

Ana Başlıklar:

Klinik Kimya

Dergi:

Ahi Evran Tıp Dergisi Vol.9 Issue 2, pp.186-194

Belge Tipi:

Makale

Yayın Tarihi:

8/2025

Belge Dili:

Türkçe

Document ID (Org No.):

2001345471

pISSN:

2619-9203

apoptosis

capsaicin

endometrial cancer

endoplasmic reticulum stressapoptoz

endometriyal kanser

endoplazmik retikulum stresi

kapsaisin

Sayı

Makale detayları

Yazarlar: Betül Keyif | Ceyhan Hacıoğlu

Yayıncı: Kirsehir Ahi Evran University

Ana Başlıklar: Klinik Kimya

Dergi: Ahi Evran Tıp Dergisi Vol.9 Issue 2, pp.186-194

Belge Tipi: Makale

Yayın Tarihi: 8/2025

Belge Dili: Türkçe

Document ID (Org No.): 2001345471

pISSN: 2619-9203

Sayı

Yazarlar:

Betül Keyif | Ceyhan Hacıoğlu

Yayıncı:

Kirsehir Ahi Evran University

Ana Başlıklar:

Klinik Kimya

Dergi:

Ahi Evran Tıp Dergisi Vol.9 Issue 2, pp.186-194

Belge Tipi:

Makale

Yayın Tarihi:

8/2025

Belge Dili:

Türkçe

Document ID (Org No.):

2001345471

pISSN:

2619-9203