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Afzelin induces immunogenic cell death against lung cancer by targeting NQO2
Lei Xia1, Xiaoqing Xu2, Meijun Li3
1Department of Medical Oncology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, No. 16369, Jingshi Road, Jinan, Shandong, 250000, China.
Background:
Lung cancer is one of the most common malignant cancers worldwide. Previous studies have shown that Afzelin, a flavonoid, possesses anticancer activity. The aim of this study was to explore Afzelin's effect on lung cancer cells and delineate potential anti-cancer mechanism.
Methods:
The effect of Afzelin on cell viability, proliferation, and apoptosis of lung cancer cells i.e., A549 and H1299 cells, was studied. The targets for Afzelin in lung cancer were predicted using SwissTargetPrediction, Next, the GO analysis and pathway enrichment were analyzed using String. For in vitro studies, the overexpression plasmid of NQO2, the identified target of Afzelin, was transfected into Afzelin-treated cells to verify the regulatory role of Afzelin on its target and signaling pathway.
Results:
In in vitro studies, Afzelin markedly inhibited cell viability, proliferation, and raised apoptotic rate of A549 and H1299 cells. In addition, Afzelin activated endoplasmic reticulum (ER) stress and increased ATP, HMGB1, and CRT levels in lung cancer cells, indicating that Afzelin induced immunogenic cell death (ICD). SwissTargetPrediction identified NQO2 as a target of Afzelin. Further, Afzelin markedly inhibited NQO2 protein expression and in turn, overexpression of NQO2 attenuated the effect of Afzelin on A549 and H1299 cells.
Conclusion:
Afzelin inhibits lung cancer progression by targeting NQO2, in turn, activating ER stress and inducing ICD.
Insights
Afzelin, a flavonoid, inhibits lung cancer cell growth and triggers cell death by targeting NQO2. This mechanism involves activating endoplasmic reticulum stress and inducing immunogenic cell death, offering a potential therapeutic strategy for lung cancer.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Lung cancer is a leading global malignancy.
- Afzelin, a flavonoid, exhibits known anticancer properties.
- Understanding Afzelin's precise anti-lung cancer mechanisms is crucial.
Purpose of the Study:
- To investigate Afzelin's impact on lung cancer cell lines (A549 and H1299).
- To elucidate the molecular targets and pathways involved in Afzelin's anti-cancer effects.
- To explore Afzelin's potential to induce immunogenic cell death.
Main Methods:
- Assessed Afzelin's effects on cell viability, proliferation, and apoptosis in vitro.
- Utilized SwissTargetPrediction to identify Afzelin's molecular targets.
- Performed Gene Ontology (GO) and pathway enrichment analyses.
- Verified NQO2 as a target via gene transfection and protein expression studies.
Main Results:
- Afzelin significantly reduced lung cancer cell viability and proliferation while increasing apoptosis.
- Afzelin induced endoplasmic reticulum (ER) stress, evidenced by increased ATP, HMGB1, and CRT levels.
- NQO2 was identified as a direct target of Afzelin, and its inhibition was key to Afzelin's effects.
Conclusions:
- Afzelin demonstrates potent anti-lung cancer activity by targeting NQO2.
- The mechanism involves the activation of ER stress and induction of immunogenic cell death (ICD).
- Afzelin represents a promising therapeutic agent for lung cancer treatment.
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