Objective To investigate the effects of Jinfukang on the growth of human lung cancer H358 cell xenografts in nude mice and its regulatory role in the TRIM52-mediated Wnt/β-catenin signaling pathway.Methods Human lung cancer H358 cells were cultured,and a subcutaneous xenograft model was established in nude mice.The mice were randomly divided into four groups:0.9％sodium chloride solution,cisplatin(3 mg·kg-1,intraperitoneal injection every 3 days),Jinfukang(0.4 mL,daily oral administration),and Jinfukang combined with cisplatin.Each group included 6 mice.After 15 days of continuous treatment,the tumor growth inhibition rate was calculated.Hematoxylin and eosin(H&E)staining was performed to observe tumor histopathological changes.TUNEL assay was used to evaluate apoptosis and calculate the apoptotic index.The relative mRNA expression levels and protein expression of TRIM52,PCNA,c-Myc,β-catenin,and Cyclin D1 were assessed by Real-time PCR and western blot,respectively.Results Compared with the saline group,Jinfukang,cisplatin,and Jinfukang combined with cisplatin treatments significantly inhibited tumor growth(P＜0.05).The combination group exhibited the most pronounced anti-tumor effect,slightly better than cisplatin alone,although the difference was not statistically significant(P＞0.05).Histopathological analysis and apoptosis indices revealed that the combination group showed the most severe necrosis and the highest level of apoptosis compared to other groups(P＜0.05).Furthermore,the combination group significantly downregulated the mRNA(P＜0.05)and protein(P＜0.05)expression levels of Cyclin D1,PCNA,TRIM52,β-catenin and c-Myc.Conclusion Jinfukang effectively inhibits the growth of human lung cancer H358 xenografts,disrupts tumor cell structure,and promotes apoptosis.Its anti-tumor effect is further enhanced when combined with cisplatin.The underlying mechanism may involve the downregulation of TRIM52 expression,leading to the suppression of Wnt/β-catenin signaling pathway activity and augmentation of anti-tumor efficacy.

Objective To investigate the effects of Jinfukang on the growth of human lung cancer H358 cell xenografts in nude mice and its regulatory role in the TRIM52-mediated Wnt/β-catenin signaling pathway.Methods Human lung cancer H358 cells were cultured,and a subcutaneous xenograft model was established in nude mice.The mice were randomly divided into four groups:0.9％sodium chloride solution,cisplatin(3 mg·kg-1,intraperitoneal injection every 3 days),Jinfukang(0.4 mL,daily oral administration),and Jinfukang combined with cisplatin.Each group included 6 mice.After 15 days of continuous treatment,the tumor growth inhibition rate was calculated.Hematoxylin and eosin(H&E)staining was performed to observe tumor histopathological changes.TUNEL assay was used to evaluate apoptosis and calculate the apoptotic index.The relative mRNA expression levels and protein expression of TRIM52,PCNA,c-Myc,β-catenin,and Cyclin D1 were assessed by Real-time PCR and western blot,respectively.Results Compared with the saline group,Jinfukang,cisplatin,and Jinfukang combined with cisplatin treatments significantly inhibited tumor growth(P＜0.05).The combination group exhibited the most pronounced anti-tumor effect,slightly better than cisplatin alone,although the difference was not statistically significant(P＞0.05).Histopathological analysis and apoptosis indices revealed that the combination group showed the most severe necrosis and the highest level of apoptosis compared to other groups(P＜0.05).Furthermore,the combination group significantly downregulated the mRNA(P＜0.05)and protein(P＜0.05)expression levels of Cyclin D1,PCNA,TRIM52,β-catenin and c-Myc.Conclusion Jinfukang effectively inhibits the growth of human lung cancer H358 xenografts,disrupts tumor cell structure,and promotes apoptosis.Its anti-tumor effect is further enhanced when combined with cisplatin.The underlying mechanism may involve the downregulation of TRIM52 expression,leading to the suppression of Wnt/β-catenin signaling pathway activity and augmentation of anti-tumor efficacy.