AIM:This study aims to investigate the effect of Agaricus blazei extract FA-2-b-β on ferroptosis of Burkitt lymphoma cells and its mechanism.METHODS:Burkitt lymphoma cell lines Raji and CA46 were treated with FA-2-b-β alone and in combination with ferrostatin-1,a ferroptosis inhibitor,or Stattic,a signal transducer and activator of transcription 3(STAT3)inhibitor.Cell viability was assessed using the CCK-8 method,and the half-maximal inhibitory concentration(IC50)of FA-2-b-β was calculated.Flow cytometry was used to detect apoptosis,cell cycle,mitochondrial membrane potential,and reactive oxygen species(ROS).Additionally,malondialdehyde(MDA)and glutathione(GSH)levels were measured using kits.The mRNA and protein expression levels of ferroptosis-related molecules were determined by RT-qPCR and Western blot.RESULTS:The extract FA-2-b-β at different concentrations significantly inhibited the proliferation of Raji and CA46 cells(P＜0.05),promoted their death,regulated cell arrest in G0/G1 phase,and decreased the mitochondrial membrane potential.(2)ROS and MDA levels were significantly increased with different concentrations of the extract FA-2-b-β(P＜0.05),while the GSH content was significantly decreased(P＜0.05).(3)The protein and mRNA levels of signal transducer and activator of transcription 3(STAT3),p-STAT3,and glutathione peroxidase 4(GPX4)were down-regulated at different concentrations of the extract FA-2-b-β.In addition,prostaglandin-endoperoxide synthase 2(PTSG2)and transferrin receptor protein 1(TfR1)protein and mRNA were up-regulated(P＜0.05),while the protein and mRNA levels of solute carrier family 7 member 11(SLC7A11)were not significantly changed.CONCLU-SION:The extract FA-2-b-β can induce ferroptosis in burkitt lymphoma,and the mechanism may be related to the inhibi-tion of STAT3/GPX4 signaling pathway.

AIM:This study aims to investigate the effect of Agaricus blazei extract FA-2-b-β on ferroptosis of Burkitt lymphoma cells and its mechanism.METHODS:Burkitt lymphoma cell lines Raji and CA46 were treated with FA-2-b-β alone and in combination with ferrostatin-1,a ferroptosis inhibitor,or Stattic,a signal transducer and activator of transcription 3(STAT3)inhibitor.Cell viability was assessed using the CCK-8 method,and the half-maximal inhibitory concentration(IC50)of FA-2-b-β was calculated.Flow cytometry was used to detect apoptosis,cell cycle,mitochondrial membrane potential,and reactive oxygen species(ROS).Additionally,malondialdehyde(MDA)and glutathione(GSH)levels were measured using kits.The mRNA and protein expression levels of ferroptosis-related molecules were determined by RT-qPCR and Western blot.RESULTS:The extract FA-2-b-β at different concentrations significantly inhibited the proliferation of Raji and CA46 cells(P＜0.05),promoted their death,regulated cell arrest in G0/G1 phase,and decreased the mitochondrial membrane potential.(2)ROS and MDA levels were significantly increased with different concentrations of the extract FA-2-b-β(P＜0.05),while the GSH content was significantly decreased(P＜0.05).(3)The protein and mRNA levels of signal transducer and activator of transcription 3(STAT3),p-STAT3,and glutathione peroxidase 4(GPX4)were down-regulated at different concentrations of the extract FA-2-b-β.In addition,prostaglandin-endoperoxide synthase 2(PTSG2)and transferrin receptor protein 1(TfR1)protein and mRNA were up-regulated(P＜0.05),while the protein and mRNA levels of solute carrier family 7 member 11(SLC7A11)were not significantly changed.CONCLU-SION:The extract FA-2-b-β can induce ferroptosis in burkitt lymphoma,and the mechanism may be related to the inhibi-tion of STAT3/GPX4 signaling pathway.

The prevention and treatment of tumor metastasis can significantly improve the survival of patients with solid tumors. However, there is still a lack of effective drugs for the prevention and treatment of metastasis. The main reason is that the existing intervention and therapeutic drugs are difficult to achieve precise prevention and treatment of metastasis. Due to disseminated tumor cells (DTCs) already exist in the metastatic target organs of early postoperative patients, they are difficult to be detected with existing imaging techniques, and there is a lack of effective intervention drugs and efficacy evaluation systems. When DTCs grow to be detectable by imaging, the patient is already in the advanced stage of cancer, which has become a bottleneck restricting the breakthroughs in metastasis prevention and treatment. This paper reviews the dormancy and survival mechanism of DTCs in metastatic target organs and its intervention strategies, in order to promote the curative effect of metastasis prevention and treatment.