Introduction To identify differentially expressed genes (DEGs) and signaling pathways in cisplatin-resistant endometrial cancer (EC) cells.
Methods Cisplatin-resistant endometrial cancer cells were established through continuous treatment of endometrial cancer cells (RL95–2 and Ishikawa) with gradually escalating doses of cisplatin. RNA-seq was performed on both original and cisplatin-resistant EC cells to evaluate DEGs. Gene-set enrichment analysis (GSEA) was also performed to find biologic processes or pathways in relation to cisplatin resistance.
Results Common hallmark gene sets enriched in both cisplatin-resistant RL95–2 and Ishikawa include inflammatory response, epithelial-mesenchymal transition, and KRAS signaling_up. Common DEGs include EMP3, CD70, and SERPINE1 in the inflammatory response gene set; LAMA2, BDNF, OXTR, CDH2, VIM, MATN3, ABI3BP, EDIL3, EMP3, CXCL1, SERPINE1, and IL32 in the epithelial-mesenchymal transition gene set; PTPRR, MMD, and KCNN4 in the KRAS signaling_up gene set.
Conclusion/Implications We identified DEGs and several pathways enriched in cisplatin-resistant EC cells as potential therapeutic targets of cisplatin resistance, which need further validation.
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