Combinatorial chemistry & high throughput screening · 2026
Arctigenin Induces Mitochondrial Apoptosis in Ovarian Cancer Cells by Downregulating Bcl2L12 Expression.
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Yang Ying, Cui Peng, Chen Weiyan, Wang Qun, Ji Tianmin, Wang Jiaxin, Zhao Jiao, Song Nan
Аннотация
INTRODUCTION: Ovarian cancer remains one of the most lethal gynecological malignancies because of late diagnosis, drug resistance, and limited treatment efficacy. This study explored the anti-apoptotic role of BCL2-like protein 12 (BCL2L12) and whether arctigenin induces apoptosis by targeting BCL2L12.
METHODS: SK-OV-3 and OVCAR-3 ovarian cancer cells were subjected to BCL2L12 knockdown or overexpression. Cell viability, proliferation, and apoptosis were evaluated by CCK-8, colony formation, and Annexin V/PI flow cytometry. Mitochondrial membrane potential and reactive oxygen species (ROS) levels were assessed using JC-1 and DCFH-DA staining, respectively, and apoptosis- and autophagy-related proteins were examined by western blotting. Public databases (TCGA, GTEx, CSIOVDB, Kaplan-Meier Plotter) were used to evaluate BCL2L12 expression and prognosis.
RESULTS: BCL2L12 was markedly upregulated in ovarian cancer and correlated with advanced stage and poor survival. Silencing BCL2L12 reduced cell growth, disrupted mitochondrial homeostasis, increased ROS accumulation, and enhanced caspase-3/7-dependent apoptosis while inhibiting autophagy. Arctigenin inhibited cell proliferation, downregulated BCL2L12, and induced mitochondrial apoptosis accompanied by ROS elevation and caspase-3/7 activation, whereas BCL2L12 overexpression attenuated these effects.
DISCUSSION: BCL2L12 acts as an anti-apoptotic factor in ovarian cancer by maintaining mitochondrial integrity and suppressing caspase-3/7 activation. Arctigenin overcomes this survival advantage by suppressing BCL2L12 and triggering mitochondrial apoptosis. Limitations include validation only in two cell lines and the lack of direct enzymatic assays for caspase-3/7 activity.
CONCLUSION: Arctigenin induces mitochondrial apoptosis in ovarian cancer by downregulating BCL2L12, supporting its potential as a low-toxicity therapeutic candidate.
METHODS: SK-OV-3 and OVCAR-3 ovarian cancer cells were subjected to BCL2L12 knockdown or overexpression. Cell viability, proliferation, and apoptosis were evaluated by CCK-8, colony formation, and Annexin V/PI flow cytometry. Mitochondrial membrane potential and reactive oxygen species (ROS) levels were assessed using JC-1 and DCFH-DA staining, respectively, and apoptosis- and autophagy-related proteins were examined by western blotting. Public databases (TCGA, GTEx, CSIOVDB, Kaplan-Meier Plotter) were used to evaluate BCL2L12 expression and prognosis.
RESULTS: BCL2L12 was markedly upregulated in ovarian cancer and correlated with advanced stage and poor survival. Silencing BCL2L12 reduced cell growth, disrupted mitochondrial homeostasis, increased ROS accumulation, and enhanced caspase-3/7-dependent apoptosis while inhibiting autophagy. Arctigenin inhibited cell proliferation, downregulated BCL2L12, and induced mitochondrial apoptosis accompanied by ROS elevation and caspase-3/7 activation, whereas BCL2L12 overexpression attenuated these effects.
DISCUSSION: BCL2L12 acts as an anti-apoptotic factor in ovarian cancer by maintaining mitochondrial integrity and suppressing caspase-3/7 activation. Arctigenin overcomes this survival advantage by suppressing BCL2L12 and triggering mitochondrial apoptosis. Limitations include validation only in two cell lines and the lack of direct enzymatic assays for caspase-3/7 activity.
CONCLUSION: Arctigenin induces mitochondrial apoptosis in ovarian cancer by downregulating BCL2L12, supporting its potential as a low-toxicity therapeutic candidate.