Background/Aim. Cellular reprogramming is driven by coordinated transcriptional and signaling changes that promote the acquisition of pluripotency-associated features. SPRY2, a negative-feedback regulator of growth factor-mediated MAPK/ERK signaling, may contribute to the pluripotency-associated cell-state transitions. This study aimed to investigate molecular pathways and regulatory networks associated with SPRY2 using an integrative bioinformatic approach. Methods. The GEO dataset GSE90895 was analyzed as a murine reprogramming model comprising mouse embryonic fibroblasts, early OSKM-induced stages, pre-induced pluripotent stem cells, and embryonic stem cells. Transcriptomic analysis in R included preprocessing, principal component analysis, differential expression, Gene Ontology and KEGG enrichment, SPRY2-focused correlation analysis, and gene-concept network construction. SPRY2 protein characterization was performed using STRING, AlphaFold, ExPASy ProtParam, and InterPro. Results. Transcriptomic profiling revealed sample heterogeneity, while PCA separated samples by distinct cellular states. Expression analysis showed higher levels of pluripotency-associated Sox2 and Myc, whereas Nanog displayed lower expression, suggesting uneven activation of pluripotency-related programs. Differential expression analysis identified 36 significantly altered genes among 33,297 transcripts. Despite this limited number, enrichment analysis indicated functional coherence, with associations involving cell differentiation, ERK1/ERK2 regulation, protein phosphorylation, receptor tyrosine kinase signaling, and epithelial remodeling. Gene-concept and protein-protein interaction analyses positioned SPRY2 within networks related to MAPK/ERK modulation and growth factor receptor signaling. Correlation and structural-functional analyses further supports SPRY2 as a candidate regulatory node linking signaling-dependent regulation with transcriptional programs involved in cellular plasticity and reprogramming. Conclusions. Molecular networks associated with SPRY2 were linked to the receptor tyrosine kinase signaling, MAPK/ERK regulation, differentiation, and cellular state remodeling during reprogramming. SPRY2 may represent a candidate negativefeedback node connecting signaling changes with transcriptional programs involved in somatic-to-pluripotent-like transitions. Based on a single public dataset and in silico analysis, these findings remain hypothesis-generating and require independent validation.