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Despite the fact that studies have revealed mechanisms underlying tumor chemoresistance, the functions of numerous potential chemoresistance-associated genes have yet to be elucidated. A bioinformatics analysis was conducted to screen differentially expressed genes (DEGs) across four types of chemoresistant tumors and functional enrichment analysis was used to examine the biological significance of these genes. Furthermore, a gene network was constructed using weighted gene co-expression network analysis to identify hub genes. A total of 6,015, 2,074, 2,141 and 954 differentially expressed genes were identified in estrogen receptor-negative breast cancer, ovarian cancer, rectal cancer and gastric cancer, respectively; however, only five of these DEGs were dysregulated in all four types of cancer. Functional enrichment analysis of the DEGs suggested that genomic stability and immune response are crucial determinants of tumor chemoresistance. In addition, 14, 8, 6 and 1 co-expressed gene modules were identified in estrogen receptor-negative breast cancer, ovarian cancer, rectal cancer and gastric cancer, respectively, and protein-protein interaction networks were created. The analysis identified only calcium-calmodulin-dependent protein kinase kinase 2, erythropoietin receptor, mitochondrial poly(A) RNA polymerase, α-parvin, and zinc finger and BTB domain-containing protein 44 to be dysregulated in all four cancer types, indicating varying mechanisms of chemoresistance in different tumor types. Furthermore, our analysis suggests that type I collagen α1, fibroblast growth factor 14 and major histocompatibility complex, class II, DR β1 potentially serve key roles in the development of chemoresistance. In conclusion, the present study proposes a simple and effective strategy for identifying genes involved in chemoresistance and predicting their potential functional roles, which may guide subsequent experimental studies. [ABSTRACT FROM AUTHOR]

Drug resistance is a primary cause of chemotherapeutic failure; however, how this resistance develops is complex. A comprehensive understanding of chemotherapeutic resistance mechanisms may aid in identifying more effective drugs and improve the survival rates of patients with cancer. Insulin-like growth factor 1 receptor (IGF1R), a member of the insulin receptor family, has been extensively assessed for biological activity, and its putative contribution to tumor cell development and progression. Furthermore, researchers have attended to drugs that target IGF1R since IGF1R functions as a membrane receptor. However, how IGF1R participates in chemotherapeutic resistance remains unclear. Therefore, the present study described the IGF1R gene and its associated signaling pathways, and offered details of IGF1R-induced tumor chemoresistance associated with promoting cell proliferation, inhibition of apoptosis, regulation of ATP-binding cassette transporter proteins and interactions with the extracellular matrix. The present study offered additional explanations for tumor chemotherapy resistance and provided a theoretical basis of IGF1R and its downstream pathways for future possible chemotherapy treatment options. [ABSTRACT FROM AUTHOR]