Objective To elucidate the functional role and underlying mechanisms of the ribosome biogenesis factor BMS1 in neuroblastoma(NB)cellular proliferation.Methods We utilized the R2 genomics analysis and visualization platform to analyze the correlation between BMS1 expression levels and clinical characteristics of NB children.The BMS1 mRNA level in three human neuroblastoma cells SK-N-BE(2),BE(2)-C,IMR-32 and two normal cells hTERT RPE-1,IMR-90 was detected by real-time quantitative polymerase chain reaction(RT-qPCR).Two distinct small interfering RNA(siRNA)sequences were used to target BMS1 mRNA in NB cells SK-N-BE(2)and BE(2)-C,with normal cells hTERT RPE-1 serving as controls.We used RT-qPCR to quantify the mRNA levels of BMS1 and two key neuroblastoma-associated molecules(MYCN and p53).After transfection with siRNA,cellular proliferation was detected by various experimental approaches:crystal violet staining,real-time cell analysis(RTCA),colony-forming unit assay and immunofluorescence.Results By analyzing two independent neuroblastoma clinical cohorts(GSE85047/NRC-283 and Westermann-144 datasets),it was found that the BMS1 mRNA level in MYCN-amplified NB was significantly higher than that in MYCN-non-amplified NB(P<0.05).Furthermore,the overall survival rate of NB children in the BMS1 high-expression group was decreased(P<0.05).Consistent with these clinical observations,the BMS1 mRNA level in NB cells SK-N-BE(2),BE(2)-C and IMR-32 was significantly higher than that in normal cells hTERT RPE-1,IMR-90(P<0.05).The targeted transient knockdown of BMS1 in NB cell lines SK-N-BE(2)and BE(2)-C resulted in decreased intracellular MYCN mRNA expression levels(P<0.05),significantly reduced cell proliferation capacity and colony-forming ability(P<0.05).Immunofluorescence revealed that the expression of Ki-67,a proliferation marker,was decreased(P<0.05).At the molecular level,RT-qPCR showed that the p53 mRNA level was significantly elevated in the BMS1-knockdown groups(si BMS1-1#and si BMS1-2#)compared with the control group(P<0.05).However,transient knockdown of BMS1 had no significant impact on the proliferative capacity of normal cells hTERT RPE-1.Conclusion BMS1 expression was up-regulated in MYCN-amplified NB and negatively correlated with the prognosis of the NB children.Mechanistically,interfering with BMS1 expression may transcriptionally activate p53 in NB cells,thereby inhibiting their proliferative ability,while having minimal impact on normal cells growth kinetics.These findings suggest that BMS1 serves as an important proliferation driver in NB and is expected to be a promising therapeutic target for NB children,particularly MYCN-amplified pediatric patients.

Objective:To investigate the clinical characteristics of children with severe human metapneumovirus (HMPV) infection and identify the risk factors associated with critical illness.Methods:A retrospective cohort study was conducted, enrolling 157 hospitalized children with severe HMPV infection, who tested positive for HMPV nucleic acid via PCR-capillary electrophoresis fragment analysis of nasopharyngeal secretions at Shanghai Children′s Hospital from January 2021 to December 2023.Clinical features, co-infections, treatment, and outcomes were collected. Based on the diagnostic criteria for severe HMPV infection, the patients were categorized into a critical illness group and a non-critical illness group. Intergroup comparisons were performed using the χ2 test or the Mann-Whitney U test. Multivariate Logistic regression analysis was employed to identify risk factors for critical HMPV infection and to establish a predictive model.The performance of the model was evaluated using receiver operating characteristic (ROC) curve analysis and calibration curves. Results:Among the 157 cases of severe HMPV infection, there were 67 males and 90 females, with an onset age of 39.0 (20.0, 55.5) months. Single-pathogen infection was observed in 125 cases (79.6%), while mixed infections accounted for 32 cases (20.4%).Severe pneumonia was diagnosed in 136 cases (86.6%).The predominant manifestations of severe HMPV infection included fever 152 cases (96.8%), cough 151 cases (96.2%), and wheezing 94 cases (59.9%).Sixty-eight patients (43.3%) required non-invasive respiratory support, 58 cases (36.9%) were admitted to the intensive care unit, and 22 cases (14.0%) underwent mechanical ventilation. Of the total, 149 cases (94.9%) were discharged with improvement, 8 cases (5.1%) were discharged against medical advice, and there were no fatal cases. The cohort was further stratified into a critical illness group 31 cases and a non-critical illness group 126 cases. Compared to the non-critical illness group, the critical illness group exhibited significantly higher rates of respiratory distress, lethargy, and intercostal retractions, along with a higher proportion of underlying comorbidities, and elevated levels of C-reactive protein and procalcitonin (all P<0.05).Conversely, albumin and hemoglobin levels were significantly lower in the critical illness group (both P<0.05). ROC curve analysis revealed that the optimal cutoff value for the duration of fever in predicting severe HMPV infection was 4.5 days.The multivariate binary Logistic regression analysis revealed that prolonged fever duration (>4.5 days) ( OR=28.00, 95% CI 5.09-153.93, P<0.001), anorexia ( OR=11.72, 95% CI 1.26-108.75, P=0.030), and immune dysfunction ( OR=36.71, 95% CI 1.55-867.31, P=0.026) were independent risk factors for severe HMPV infection. A predictive model for critical illness was constructed based on these independent risk factors. ROC curve analysis demonstrated excellent discriminative ability, with an area under the curve of 0.96 (95% CI 0.92-1.00, P<0.001). The optimal predictive probability threshold was 0.17, yielding a sensitivity of 0.93 and specificity of 0.92. The calibration curve closely approximated the ideal curve, indicating good model calibration ( P=0.157). Conclusions:Severe HMPV infection is predominantly observed as a single infection and is prone to progress to severe pneumonia, with fever, cough, and wheezing as the main clinical manifestations. A subset of cases progresses to critical illness, though the overall prognosis is favorable. Prolonged fever duration (>4.5 days), anorexia, and immune dysfunction were independent risk factors for critical illness.The risk prediction model constructed for pediatric critical HMPV infection demonstrated robust discriminative ability with excellent calibration.

Objective To explore the function of olfactomedin domain family protein 3(OLFM3)in neuroblastoma(NB).Methods The relationship between the expression of OLFM3 mRNA and v-myc avian myelocytomatosis viral oncogene neuroblastoma derived homolog(MYCN)amplification status and the prognosis of patients in NB clin-ical samples were clarified by using R2 Genomics Analysis and Visualization Platform.Depmap database was used to examine the expression level of OLFM3 in different tumors cell lines and to identify the correlation between OLFM3 expression and MYCN amplification status in various NB cell lines.RT-qPCR and Western blot were used to detect the knockdown level of OLFM3.Cell proliferation was monitored using crystal violet staining and real?time cellular analysis.The colony formation ability of NB cells was assessed using colony?forming unit assay.Results Analysis of R2 database revealed higher level of OLFM3 expression in MYCN?amplified NB clinical samples(P<0.001).Patients with high OLFM3 expression showed a significantly lower overall survival probability compared to those with low OLFM3 expression(P<0.05).Analysis with Depmap database revealed that the expres?sion level of OLFM3 was higher in NB than that in other kind of tumor.The expression level of OLFM3 was signifi?cantly higher in the MYCN?amplified cell lines than in the MYCN?non?amplified cell lines(P<0.01).In MYCN?am?plified NB cells,knockdown of OLFM3 inhibited cells proliferation(P<0.001)and colony formation(P<0.001),but there was no noticeable changes observed in MYCN?non?amplified cells.Conclusions OLFM3 specifically pro?motes the proliferation of MYCN?amplified NB cells,but has a less effect on MYCN?non?amplified cells,indicating it is a potential biomarker for high?risk MYCN?amplified NB.

Objective:To analyze the distribution and epidemiological characteristics of non-bacterial pathogens in hospitalized children with acute respiratory infections at a tertiary pediatric hospital in Shanghai during 2023.Methods:A retrospective study was conducted on 10 591 children with acute respiratory tract infections who were hospitalized in Shanghai Children's Hospital from January to December 2023. A multiplex PCR combined with capillary electrophoresis platform was used to detect 11 common non-bacterial respiratory pathogens（including viruses and atypical pathogens）. Statistical analysis was carried out using SPSS 29.0 software. Qualitative data were presented as numbers and percentages，and the Chi-square test was employed to make comparisons between groups，aiming to analyze the differences in the distribution of different pathogens according to gender，age group，and season. Additionally，based on the severity of the disease，patients were calssified into a severe pneumonia group and a non-severe pneumonia group to further explore the characteristics of the pathogen spectrum of severe pneumonia.Results:The total detection rate of pathogens was 54.39%（5 760/10 591），and the proportion of mixed infections was 12.76%（735/5 760）. The dominant pathogens and their proportions were as follows： Mycoplasma pneumoniae（19.20%，2 034/10 591），human rhinovirus（12.16%，1 288/10 591），influenza A virus（8.31%，880/10 591），and respiratory syncytial virus（8.14%，862/10 591）. Epidemiological characteristics showed that：（1）In terms of age： Mycoplasma pneumoniae was more common in older children（29.55%，901/3 049，in the school-age group，χ 2 = 653.67， P<0.001）. Influenza A virus had a high incidence in the adolescent group（11.34%，45/397，χ 2=48.69， P<0.001）. Respiratory syncytial virus was most susceptible in the infant group（20.94%，280/1 337，χ 2=739.92， P<0.001）. Human rhinovirus showed the characteristic of general susceptibility across all ages.（2）Monthly and seasonal distribution： Mycoplasma pneumoniae had a seasonal epidemic in summer and autumn（it began to rise in May and peaked in October at 34.22%，439/1 283）；influenza A virus had a bimodal distribution in spring and winter（the peak was 37.15% in March，315/848）；respiratory syncytial virus had a dominant epidemic in spring and summer（the detection rate was 21.24% in May，206/970），and human rhinovirus was prevalent throughout the year.（3）Clinical correlation：The detection rate of pathogens in the severe pneumonia group was significantly higher than that in the non-severe group：84.19%（426/506） vs 2.89%（5 334/10 085），χ 2=56.23， P<0.001. Conclusions:In 2023，the pathogen spectrum of hospitalized children with acute respiratory infections in the Shanghai area exhibits an epidemic pattern dominated by Mycoplasma pneumoniae，and its transmission dynamics are significantly age-dependent. This study delineates the pathogen-host-environment tripartite interactions，establishing an evidence-based foundation for formulating precision diagnostic-therapeutic algorithms and seasonal nosocomial infection prevention frameworks.

Objective To elucidate the functional role and underlying mechanisms of the ribosome biogenesis factor BMS1 in neuroblastoma(NB)cellular proliferation.Methods We utilized the R2 genomics analysis and visualization platform to analyze the correlation between BMS1 expression levels and clinical characteristics of NB children.The BMS1 mRNA level in three human neuroblastoma cells SK-N-BE(2),BE(2)-C,IMR-32 and two normal cells hTERT RPE-1,IMR-90 was detected by real-time quantitative polymerase chain reaction(RT-qPCR).Two distinct small interfering RNA(siRNA)sequences were used to target BMS1 mRNA in NB cells SK-N-BE(2)and BE(2)-C,with normal cells hTERT RPE-1 serving as controls.We used RT-qPCR to quantify the mRNA levels of BMS1 and two key neuroblastoma-associated molecules(MYCN and p53).After transfection with siRNA,cellular proliferation was detected by various experimental approaches:crystal violet staining,real-time cell analysis(RTCA),colony-forming unit assay and immunofluorescence.Results By analyzing two independent neuroblastoma clinical cohorts(GSE85047/NRC-283 and Westermann-144 datasets),it was found that the BMS1 mRNA level in MYCN-amplified NB was significantly higher than that in MYCN-non-amplified NB(P<0.05).Furthermore,the overall survival rate of NB children in the BMS1 high-expression group was decreased(P<0.05).Consistent with these clinical observations,the BMS1 mRNA level in NB cells SK-N-BE(2),BE(2)-C and IMR-32 was significantly higher than that in normal cells hTERT RPE-1,IMR-90(P<0.05).The targeted transient knockdown of BMS1 in NB cell lines SK-N-BE(2)and BE(2)-C resulted in decreased intracellular MYCN mRNA expression levels(P<0.05),significantly reduced cell proliferation capacity and colony-forming ability(P<0.05).Immunofluorescence revealed that the expression of Ki-67,a proliferation marker,was decreased(P<0.05).At the molecular level,RT-qPCR showed that the p53 mRNA level was significantly elevated in the BMS1-knockdown groups(si BMS1-1#and si BMS1-2#)compared with the control group(P<0.05).However,transient knockdown of BMS1 had no significant impact on the proliferative capacity of normal cells hTERT RPE-1.Conclusion BMS1 expression was up-regulated in MYCN-amplified NB and negatively correlated with the prognosis of the NB children.Mechanistically,interfering with BMS1 expression may transcriptionally activate p53 in NB cells,thereby inhibiting their proliferative ability,while having minimal impact on normal cells growth kinetics.These findings suggest that BMS1 serves as an important proliferation driver in NB and is expected to be a promising therapeutic target for NB children,particularly MYCN-amplified pediatric patients.

Objective:To analyze the distribution and epidemiological characteristics of non-bacterial pathogens in hospitalized children with acute respiratory infections at a tertiary pediatric hospital in Shanghai during 2023.Methods:A retrospective study was conducted on 10 591 children with acute respiratory tract infections who were hospitalized in Shanghai Children's Hospital from January to December 2023. A multiplex PCR combined with capillary electrophoresis platform was used to detect 11 common non-bacterial respiratory pathogens（including viruses and atypical pathogens）. Statistical analysis was carried out using SPSS 29.0 software. Qualitative data were presented as numbers and percentages，and the Chi-square test was employed to make comparisons between groups，aiming to analyze the differences in the distribution of different pathogens according to gender，age group，and season. Additionally，based on the severity of the disease，patients were calssified into a severe pneumonia group and a non-severe pneumonia group to further explore the characteristics of the pathogen spectrum of severe pneumonia.Results:The total detection rate of pathogens was 54.39%（5 760/10 591），and the proportion of mixed infections was 12.76%（735/5 760）. The dominant pathogens and their proportions were as follows： Mycoplasma pneumoniae（19.20%，2 034/10 591），human rhinovirus（12.16%，1 288/10 591），influenza A virus（8.31%，880/10 591），and respiratory syncytial virus（8.14%，862/10 591）. Epidemiological characteristics showed that：（1）In terms of age： Mycoplasma pneumoniae was more common in older children（29.55%，901/3 049，in the school-age group，χ 2 = 653.67， P<0.001）. Influenza A virus had a high incidence in the adolescent group（11.34%，45/397，χ 2=48.69， P<0.001）. Respiratory syncytial virus was most susceptible in the infant group（20.94%，280/1 337，χ 2=739.92， P<0.001）. Human rhinovirus showed the characteristic of general susceptibility across all ages.（2）Monthly and seasonal distribution： Mycoplasma pneumoniae had a seasonal epidemic in summer and autumn（it began to rise in May and peaked in October at 34.22%，439/1 283）；influenza A virus had a bimodal distribution in spring and winter（the peak was 37.15% in March，315/848）；respiratory syncytial virus had a dominant epidemic in spring and summer（the detection rate was 21.24% in May，206/970），and human rhinovirus was prevalent throughout the year.（3）Clinical correlation：The detection rate of pathogens in the severe pneumonia group was significantly higher than that in the non-severe group：84.19%（426/506） vs 2.89%（5 334/10 085），χ 2=56.23， P<0.001. Conclusions:In 2023，the pathogen spectrum of hospitalized children with acute respiratory infections in the Shanghai area exhibits an epidemic pattern dominated by Mycoplasma pneumoniae，and its transmission dynamics are significantly age-dependent. This study delineates the pathogen-host-environment tripartite interactions，establishing an evidence-based foundation for formulating precision diagnostic-therapeutic algorithms and seasonal nosocomial infection prevention frameworks.

Objective:To investigate the clinical characteristics of children with severe human metapneumovirus (HMPV) infection and identify the risk factors associated with critical illness.Methods:A retrospective cohort study was conducted, enrolling 157 hospitalized children with severe HMPV infection, who tested positive for HMPV nucleic acid via PCR-capillary electrophoresis fragment analysis of nasopharyngeal secretions at Shanghai Children′s Hospital from January 2021 to December 2023.Clinical features, co-infections, treatment, and outcomes were collected. Based on the diagnostic criteria for severe HMPV infection, the patients were categorized into a critical illness group and a non-critical illness group. Intergroup comparisons were performed using the χ2 test or the Mann-Whitney U test. Multivariate Logistic regression analysis was employed to identify risk factors for critical HMPV infection and to establish a predictive model.The performance of the model was evaluated using receiver operating characteristic (ROC) curve analysis and calibration curves. Results:Among the 157 cases of severe HMPV infection, there were 67 males and 90 females, with an onset age of 39.0 (20.0, 55.5) months. Single-pathogen infection was observed in 125 cases (79.6%), while mixed infections accounted for 32 cases (20.4%).Severe pneumonia was diagnosed in 136 cases (86.6%).The predominant manifestations of severe HMPV infection included fever 152 cases (96.8%), cough 151 cases (96.2%), and wheezing 94 cases (59.9%).Sixty-eight patients (43.3%) required non-invasive respiratory support, 58 cases (36.9%) were admitted to the intensive care unit, and 22 cases (14.0%) underwent mechanical ventilation. Of the total, 149 cases (94.9%) were discharged with improvement, 8 cases (5.1%) were discharged against medical advice, and there were no fatal cases. The cohort was further stratified into a critical illness group 31 cases and a non-critical illness group 126 cases. Compared to the non-critical illness group, the critical illness group exhibited significantly higher rates of respiratory distress, lethargy, and intercostal retractions, along with a higher proportion of underlying comorbidities, and elevated levels of C-reactive protein and procalcitonin (all P<0.05).Conversely, albumin and hemoglobin levels were significantly lower in the critical illness group (both P<0.05). ROC curve analysis revealed that the optimal cutoff value for the duration of fever in predicting severe HMPV infection was 4.5 days.The multivariate binary Logistic regression analysis revealed that prolonged fever duration (>4.5 days) ( OR=28.00, 95% CI 5.09-153.93, P<0.001), anorexia ( OR=11.72, 95% CI 1.26-108.75, P=0.030), and immune dysfunction ( OR=36.71, 95% CI 1.55-867.31, P=0.026) were independent risk factors for severe HMPV infection. A predictive model for critical illness was constructed based on these independent risk factors. ROC curve analysis demonstrated excellent discriminative ability, with an area under the curve of 0.96 (95% CI 0.92-1.00, P<0.001). The optimal predictive probability threshold was 0.17, yielding a sensitivity of 0.93 and specificity of 0.92. The calibration curve closely approximated the ideal curve, indicating good model calibration ( P=0.157). Conclusions:Severe HMPV infection is predominantly observed as a single infection and is prone to progress to severe pneumonia, with fever, cough, and wheezing as the main clinical manifestations. A subset of cases progresses to critical illness, though the overall prognosis is favorable. Prolonged fever duration (>4.5 days), anorexia, and immune dysfunction were independent risk factors for critical illness.The risk prediction model constructed for pediatric critical HMPV infection demonstrated robust discriminative ability with excellent calibration.

Objective To explore the effect of open reading frame 66(C12ORF66)located at chromosome 12 on the viability of MYCN amplified NB cell lines.Methods DDatasets GSE16476 and GSE49710 in R2 database were analyzed for expression level of C12ORF66 in MYCN amplified and MYCN non-amplified NB cells and its potential correlation with the prognosis of pediatric patients.C12ORF66 mRNA expression level in normal tissue immortalized cell lines,MYCN amplified and MYCN non-amplified cell lines were detected by RT-qRCR.Transient or stable knockdown of C12ORF66 cell lines were constructed to compare the difference in real time cellular analysis(RTCA),colony formation,Ki67 positive cells between the control group and the C12ORF66 knockdown group.Results By analyzing R2 datasets,C12ORF66 level in MYCN amplified samples was significantly higher than that in MYCN non-amplified samples,and the expression of C12ORF66 was negatively correlated with the prognosis of pediatric patients(P＜0.05).C12ORF66 highly expressed in MYCN-amplified BE(2)-C and SK-N-BE(2)cell lines than in MYCN non-amplified CHLA-255 and SH-SY5Y cell lines(P＜0.001).Transient or stable knockdown of C12ORF66 resulted in significant slow down of proliferation of MYCN amplified NB cells(P＜0.001),the colony formation ability was significantly reduced(P＜0.001),and the proportion of Ki67 positive cells was significantly decreased(P＜0.05).Conclusions C12ORF66 was highly expressed in MYCN amplified clinical NB samples and cell lines which is believed to be correlated with poor prognosis of pediatric patients.C12ORF66 knockdown signifi-cantly inhibits cell viability of NB cells.

Objective To compare the effect of using the fresh tumor lump and the recovered low temperature-storing VX2 tumor lump that have been frozen for different time to construct the rabbit HCC model.Methods Fish-like fresh VX2 tumor lumps were selected.After the peripheral necrotic tissue and muscle were removed,the tumor lumps were frozen at-80℃ for 3,5 and 7 months.Twenty New Zealand white rabbits were randomly divided into 4 groups.The rabbits in group A(control group)received fresh liver tumor lump implantation to construct in-situ VX2 rabbit HCC models.The rabbits in groups B,C and D(experimental groups)received implantation of the recovered low temperature-storing VX2 tumor lump which had been frozen at-80℃ for 3,5 and 7 months,respectively,to construct in-situ VX2 rabbit HCC models.Fourteen days after implantation,the modeling effect of tumor formation in each group was assessed.The proliferation,apoptosis of tumor cells and the angiogenesis were evaluated by immunofluorescence assay.Results The tumor formation rate of all group A,B,C and D was 100％.However,with the extension of cryopreservation time,the difference in tumor mass activity became larger after 5 months,and the necrotic area of liver tumor center became enlarged.Histological examination showed that there were no significant differences in the expressions of TUNEL,Ki67,HIF-α,VEGF and CD31 between group A and group B,while there were significant differences in the expressions of TUNEL,Ki67,HIF1-α,VEGF and CD31 between group A,B and group C,D.Conclusion The rabbit VX2 HCC model,which is constructed by implantation of recovered low temperature-storing VX2 tumor lump being frozen at-80℃ in vitro for a certain time,can be successfully established within 7 months.The difference in tumor mass activity between tumor lumps became larger after 5 months.But on the whole,the constructed rabbit VX2 HCC model can better preserve the tumor strain activity.This modeling technique can save manpower and material resources.(J Intervent Radiol,2024,33:269-274)

Objective:To investigate the function and underlying mechanism of cysteine and glycine-rich protein 2(CSRP2)in neuroblastoma(NB).Methods:The correlation between the expression level of CSRP2 mRNA and the prognosis of NB children in NB clinical samples was analyzed in R2 Genomics Analysis and Visualization Platform.The small interfering RNA(siRNA)targeting CSRP2 or CSRP2 plasmid were transfected to NB cell lines SK-N-BE(2)and SH-SY5Y.Cell proliferation was observed by crystal violet staining and real-time cellular analysis.The ability of colony formation of NB cells was ob-served by colony-forming unit assay.Immunofluorescence assay was used to detect the expression of the proliferation marker Ki-67.Flow cytometry analysis for cell cycle proportion was used with cells stained by propidium iodide(PI).Annexin V/7AAD was used to stain cells and analyze the percentage of cell apoptosis.The ability of cell migration was determined by cell wound-healing assay.The level of protein and mRNA expression of CSRP2 in NB primary tumor and NB cell lines were detected by Western blot and quantitative real-time PCR(RT-qPCR).Results:By analyzing the NB clinical sample databases,it was found that the expression levels of CSRP2 in high-risk NB with 3/4 stages in international neuroblas-toma staging system(INSS)were significantly higher than that in low-risk NB with 1/2 INSS stages.The NB patients with high expression levels of CSRP2 were shown lower overall survival rate than those with low expression levels of CSRP2.We detected the protein levels of CSRP2 in the NB samples by Western blot,and found that the protein level of CSRP2 in 3/4 INSS stages was significantly higher than that in 1/2 INSS stages.Knockdown of CSRP2 inhibited cell viability and proliferation of NB cells.Overexpression of CSRP2 increased the proliferation of NB cells.Flow cytometry showed that the proportion of sub-G1,G0/G1 and S phase cells and Annexin V positive cells were increased after CSRP2 deficiency.In the cell wound-healing assay,the healing rate of NB cells was significantly attenuated after knockdown of CSRP2.Further mechanism studies showed that the proportion of the proliferation marker Ki-67 and the phospho-rylation levels of extracellular signal-regulated kinases 1/2(ERK1/2)were significantly decreased after CSRP2 knockdown.Conclusion:CSRP2 is highly expressed in high-risk NB with 3/4 INSS stages,and the expression levels of CSRP2 are negatively correlated with the overall survival of NB patients.CSRP2 significantly increased the proliferation and cell migration of NB cells and inhibited cell apoptosis via the activation of ERK1/2.All these results indicate that CSRP2 promotes the progression of NB by activating ERK1/2,and this study will provide a potential target for high-risk NB therapy.