Objective To investigate 5-aminoimidazole-4-carboxamide ribonucleotide formyl transferase/inosine monophos-phate cyclohydrolase(ATIC),a key regulator of metabolism and cell proliferation,to explore its role in glioma proliferation,e-valuate its association with patient prognosis,and elucidate the underlying molecular mechanisms.Methods Using data from The Cancer Genome Atlas(TCGA),Genotype-Tissue Expression(GTEx),and Chinese Glioma Genome Atlas(CGGA)databas-es,we analyzed differential ATIC expression between tumor tissues and adjacent normal tissues in glioma patients,as well as its correlation with clinical features including pathological grade,isocitrate dehydrogenase(IDH)mutation status,and chromosome 1p/19q deletion.ATIC was knocked down using siRNA transfection.The effect of ATIC on the proliferation of glioma cell lines(LN229,U373,and U251)was evaluated using EdU,CCK-8,and colony formation assays.Furthermore,ATIC overexpression via plasmid transfection was analyzed in conjunction with flow cytometry and Western blotting analysis to assess cell cycle pro-gression and cyclin-related protein expression.Results ATIC expression was significantly elevated in glioma tissues compared to adjacent normal tissues(P＜0.01).Patients with high ATIC expression exhibited shorter overall survival(OS)and were asso-ciated with higher pathological grades,wild-type IDH status,and the presence of chromosome 1p/19q deletion.Compared with U373 and U251 glioma cell lines,LN229 and U87 glioma cell lines demonstrated higher ATIC expression.In siRNA-mediated ATIC knockdown models(siATIC-LN229,siATIC-U373),cell proliferation was suppressed as demonstrated by EdU,CCK-8,and colony formation assays,whereas ATIC overexpression in U251 cells promoted proliferation.Flow cytometry revealed G1-phase arrest and impaired S-phase progression in siATIC-LN229 cells.Conversely,ATIC overexpression in U251 cells decreased G1-phase accumulation and increased S-phase progression.Mechanistically,ATIC knockdown decreased the expression of phos-phorylated Rb(p-Rb),upregulated p21,and downregulated key cyclin-related proteins essential for G1/S transition.In contrast,ATIC overexpression facilitated the G1/S transition through p21 downregulation and enhanced phosphorylation of Rb pro-tein.Conclusion High ATIC expression is associated with poor clinical outcomes in glioma patients and may promote tumor progression through regulation of the p21-Rb signaling pathway.Therefore,ATIC represents a promising biomarker for both clinical diagnosis and prognosis in glioma.

Objective To determine KCNJ14 gene expression in human glioma cells and assess its impact on U251 cell pro-liferation,while exploring the potential mechanism involved.Methods The protein expression levels of KCNJ14 in different hu-man glioma cell lines(U87,U251,SNB19,and LN229)were analyzed by Western blotting.KCNJ14 was knocked down and over-expressed in U251 cells using siRNA and plasmid transfection,respectively.Subsequently,protein expression levels,cell prolif-eration capacity,and the regulation of cell cycle related proteins were measured in each group.The association between KCNJ14 mRNA expression and clinical survival prognosis in glioma patients was evaluated through statistical analysis of public databas-es.Results KCNJ14 protein expression varied across different human glioma cell lines,with the highest level observed in U251 cells.Inhibition of KCNJ14 suppressed U251 cell proliferation and impaired cell cycle progression.Bioinformatics analysis re-vealed that KCNJ14 mRNA expression was significantly associated with clinical characteristics and survival outcomes in glioma patients.Conclusion KCNJ14 exhibits differential expression in glioma cells and is negatively associated with patient prognosis.Mechanistically,it may regulate glioma cell proliferation by modulating cell cycle related proteins.

Objective To investigate 5-aminoimidazole-4-carboxamide ribonucleotide formyl transferase/inosine monophos-phate cyclohydrolase(ATIC),a key regulator of metabolism and cell proliferation,to explore its role in glioma proliferation,e-valuate its association with patient prognosis,and elucidate the underlying molecular mechanisms.Methods Using data from The Cancer Genome Atlas(TCGA),Genotype-Tissue Expression(GTEx),and Chinese Glioma Genome Atlas(CGGA)databas-es,we analyzed differential ATIC expression between tumor tissues and adjacent normal tissues in glioma patients,as well as its correlation with clinical features including pathological grade,isocitrate dehydrogenase(IDH)mutation status,and chromosome 1p/19q deletion.ATIC was knocked down using siRNA transfection.The effect of ATIC on the proliferation of glioma cell lines(LN229,U373,and U251)was evaluated using EdU,CCK-8,and colony formation assays.Furthermore,ATIC overexpression via plasmid transfection was analyzed in conjunction with flow cytometry and Western blotting analysis to assess cell cycle pro-gression and cyclin-related protein expression.Results ATIC expression was significantly elevated in glioma tissues compared to adjacent normal tissues(P＜0.01).Patients with high ATIC expression exhibited shorter overall survival(OS)and were asso-ciated with higher pathological grades,wild-type IDH status,and the presence of chromosome 1p/19q deletion.Compared with U373 and U251 glioma cell lines,LN229 and U87 glioma cell lines demonstrated higher ATIC expression.In siRNA-mediated ATIC knockdown models(siATIC-LN229,siATIC-U373),cell proliferation was suppressed as demonstrated by EdU,CCK-8,and colony formation assays,whereas ATIC overexpression in U251 cells promoted proliferation.Flow cytometry revealed G1-phase arrest and impaired S-phase progression in siATIC-LN229 cells.Conversely,ATIC overexpression in U251 cells decreased G1-phase accumulation and increased S-phase progression.Mechanistically,ATIC knockdown decreased the expression of phos-phorylated Rb(p-Rb),upregulated p21,and downregulated key cyclin-related proteins essential for G1/S transition.In contrast,ATIC overexpression facilitated the G1/S transition through p21 downregulation and enhanced phosphorylation of Rb pro-tein.Conclusion High ATIC expression is associated with poor clinical outcomes in glioma patients and may promote tumor progression through regulation of the p21-Rb signaling pathway.Therefore,ATIC represents a promising biomarker for both clinical diagnosis and prognosis in glioma.

Objective To determine KCNJ14 gene expression in human glioma cells and assess its impact on U251 cell pro-liferation,while exploring the potential mechanism involved.Methods The protein expression levels of KCNJ14 in different hu-man glioma cell lines(U87,U251,SNB19,and LN229)were analyzed by Western blotting.KCNJ14 was knocked down and over-expressed in U251 cells using siRNA and plasmid transfection,respectively.Subsequently,protein expression levels,cell prolif-eration capacity,and the regulation of cell cycle related proteins were measured in each group.The association between KCNJ14 mRNA expression and clinical survival prognosis in glioma patients was evaluated through statistical analysis of public databas-es.Results KCNJ14 protein expression varied across different human glioma cell lines,with the highest level observed in U251 cells.Inhibition of KCNJ14 suppressed U251 cell proliferation and impaired cell cycle progression.Bioinformatics analysis re-vealed that KCNJ14 mRNA expression was significantly associated with clinical characteristics and survival outcomes in glioma patients.Conclusion KCNJ14 exhibits differential expression in glioma cells and is negatively associated with patient prognosis.Mechanistically,it may regulate glioma cell proliferation by modulating cell cycle related proteins.