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EP006/#881  Differential gene expressions in endometrial cancer cells with acquired cisplatin resistance
  1. Mi-Kyung Kim1,
  2. Bora Kim1 and
  3. Yun Hwan Kim2
  1. 1Ewha Womans University Mokdong Hospital, Obstetrics and Gynecology, Seoul, Korea, Republic of
  2. 2Ewha Womans University Mokdong Hospital, Ewha Womans University College of Medicine, Department of Obstetrics and Gynecology, seoul, Korea, Republic of


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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