The following is a summary of “Bioinformatic analysis of the expression profile and identification of RhoGDI2 as a biomarker in imatinib-resistant K562 cells,” published in the August 2023 issue of Hematology by Yang et al.
Aggressive chronic myeloid leukemia (CML) stems from hematopoietic cells. First-gen tyrosine kinase inhibitor (IM) enhances living quality, yet tyrosine kinase inhibitor (TKI) resistance leads to recurrence, impacting CML prognosis. Researchers performed a cohort study to identify signaling pathways and biomarkers for imatinib resistance.
They started mRNA and miRNA expression profiling in imatinib-sensitive K562 cells (IS-K562) and imatinib-resistant K562 cells (IR-K562). Differentially expressed genes (DEGs) were identified, and pathway enrichment analyses were conducted to uncover the underlying mechanisms. Protein–protein interaction (PPI) and miRNA-mRNA regulatory networks were built to reveal potential gene relationships. Further investigations involved RT-qPCR, western blot, and CCK8 assays.
The results showed 623 DEGs and 61 differentially expressed miRNAs. GO analysis highlighted cell adhesion, migration, differentiation, and inflammation roles. KEGG highlighted enrichment in Rap1 signaling, focal adhesion, proteoglycans, cancer-related transcriptional misregulation, stem cell pluripotency, and immune pathways. PPI and miRNA-mRNA networks showed diverse gene connections. RHoGDI2‘s pivotal role in imatinib resistance was confirmed.
They concluded that the interplay of genes and pathways influences TKIs resistance, with RHoGDI2 as an identified biomarker in IR-K562.
Source: tandfonline.com/doi/full/10.1080/16078454.2023.2244856
