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Background Taxol resistance in serous ovarian cancer is responsible for its poor prognosis, yet the underlying mechanism is still poorly understood. Thus, we probed the mechanism of Taxol resistance in serous ovarian cancer with multiple bioinformatic methods to provide novel insights into potential therapies. Methods The differentially expressed genes (DEGs) in Taxol-sensitive and Taxol-resistant cell lines and their relationship with the overall survival (OS) and progression-free interval (PFI) of ovarian cancer patients were analyzed using gene expression datasets from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). The role of receptor interacting serine/threonine kinase 2 ( RIPK2 ) was validated via identification of its coexpressed genes, functional analysis and generation of a protein-protein interaction (PPI) network. The single sample gene set enrichment analysis (ssGSEA) was used to explore immune infiltration, and genomic alterations of  RIPK2  were also analyzed via cBio Cancer Genomics Portal (cBioProtal). Results RIPK2  was highly expressed in Taxol resistant ovarian cancer cell lines, and its high expression was also linked with shorter OS and PFI in serous ovarian cancer patients. The PPI network analysis and pathway analysis demonstrated that  RIPK2  might participate in the positive regulation of NF-κB transcription factor activity.  RIPK2  expression was related to tumor microenvironment alterations, which might participate in the formation of Taxol resistance. Conclusions Our studies suggested that high expression of  RIPK2  is related to Taxol resistance in serous ovarian cancer, and that  RIPK2  induces Taxol resistance through NOD1/RIPK2/NF-κB inflammatory pathway activation and tumor microenvironment changes.

High expression of RIPK2 is associated with Taxol resistance in serous ovarian cancer