RESUMO
Background: The molecular mechanisms underlying gastric cancer (GC) progression are unclear. The authors examined key genes associated with the prognosis and tumor-infiltrating immune cells in patients with GC. Materials and Methods: Gene expression omnibus (GEO) was used to filter and obtain GC-related differentially expressed genes (DEGs). The molecular functions, biological processes, and cellular components of the DEGs were subjected to enrichment analysis. Protein-protein interaction networks of proteins encoded by the DEGs were analyzed using STRING. The authors also identified hub genes of GC, as well as their expression levels in GC and their relationship with patient prognosis. The relationship between hub genes and tumor-infiltrating immune cells was analyzed by Tumor IMmune Estimation Resource. Results: Six GEO datasets were included in this study, and 265 DEGs were identified. These DEGs were enriched in different signaling pathways and had different biological functions. Six hub genes were potentially significantly related to the molecular mechanisms of GC (TOP2A, FN1, SPARC, COL3A1, COL1A1, and TIMP1). These genes are potential markers of prognosis. Five hub genes were significantly positively correlated with the number of macrophages, neutrophils, and dendritic cells. Conclusions: The authors provide a theoretical basis for exploring the molecular regulation mechanism underlying GC and identifying therapeutic targets.
Assuntos
Biomarcadores Tumorais/genética , Regulação Neoplásica da Expressão Gênica/imunologia , Neoplasias Gástricas/mortalidade , Microambiente Tumoral/imunologia , Biologia Computacional , Conjuntos de Dados como Assunto , Células Dendríticas/imunologia , Gastrectomia , Mucosa Gástrica/imunologia , Mucosa Gástrica/patologia , Mucosa Gástrica/cirurgia , Humanos , Estimativa de Kaplan-Meier , Linfócitos do Interstício Tumoral/imunologia , Neutrófilos/imunologia , Prognóstico , Mapas de Interação de Proteínas/genética , Transdução de Sinais/genética , Transdução de Sinais/imunologia , Neoplasias Gástricas/genética , Neoplasias Gástricas/imunologia , Neoplasias Gástricas/cirurgia , Taxa de Sobrevida , Microambiente Tumoral/genética , Macrófagos Associados a Tumor/imunologiaRESUMO
SUMOylation is a reversible post-translational modification which has emerged as a crucial molecular regulatory mechanism, involved in the regulation of DNA damage repair, immune responses, carcinogenesis, cell cycle progression and apoptosis. Four SUMO isoforms have been identified, which are SUMO1, SUMO2/3 and SUMO4. The small ubiquitin-like modifier (SUMO) pathway is conserved in all eukaryotes and plays pivotal roles in the regulation of gene expression, cellular signaling and the maintenance of genomic integrity. The SUMO catalytic cycle includes maturation, activation, conjugation, ligation and de-modification. The dysregulation of the SUMO system is associated with a number of diseases, particularly cancer. SUMOylation is widely involved in carcinogenesis, DNA damage response, cancer cell proliferation, metastasis and apoptosis. SUMO can be used as a potential therapeutic target for cancer. In this review, we briefly outline the basic concepts of the SUMO system and summarize the involvement of SUMO proteins in cancer cells in order to better understand the role of SUMO in human disease.
