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Objective To analyze and identify hub genes of temozolomide resistance in glioma by an integrated bioinformatics approach, and to provide new directions for the study of drug resistance mechanisms and clinical treatment of glioma. Methods R-language was used to screen for differentially expressed genes (DEGs). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis was used to analyze their functions and pathways. Protein-protein interaction (PPI) analysis was used to screen for hub genes. The Gliovis database was used to verify the mRNA expression of hub genes in primary and recurrent glioma tissues and to analyze their survival. Results A total of 1 230 DEGs were screened, including 648 up-regulated genes and 582 down-regulated genes. GO showed that DEGs were involved in ribosome biogenesis, ribonucleoprotein complex biosynthesis and rRNA processing in terms of biological processes (BP). Cellular components (CC) included mitochondrial matrix, condensed chromosomes, chromosomal regions, etc. In terms of molecular functions (MF), DEGs participated in catalytic activity, acting on RNA, transferase activity, etc. KEGG showed that DEGs were mainly involved in nucleoplasmic transport, cell cycle, DNA replication, etc. PPI screened TOP10 hub genes: BUB1B, ASPM, KIF4A, CDC6, NCAPG, MCM7, MCM3, MCM5, MCM10, RFC4. Analysis of the Gliovis database showed that BUB1B, ASPM, KIF4A, CDC6, NCAPG, MCM3, MCM5, MCM10 and RFC4 were relatively up-regulated in recurrent glioma tissues and negatively correlated with survival. Conclusion BUB1B, ASPM, KIF4A, CDC6, NCAPG, MCM3, MCM5, MCM10 and RFC4, which are highly expressed in drug-resistant glioma cells and recurrent glioma tissues and negatively correlated with survival, are identified as hub genes for temozolomide resistance in glioma by comprehensive bioinformatics analysis. [ABSTRACT FROM AUTHOR]