Abstract: Objective To establish the paclitaxel-resistant gastric cancer cell(HGC-27/PTX) and investigate the changes of characteristics before and after resistance, as well as the possible resistant mechanisms. Methods The paclitaxel-resistant gastric cancer cell HGC-27/PTX was established by increasing paclitaxel dose gradually and intermittently. The IC50 (50% inhibitory concentration) and cell cycle were determined by CCK-8 assay and flow cytometry, respectively. The differentially expressed genes (DEGs) and signaling pathways were analyzed using RNAseq. Results The establishment of HGC-27/PTX cells lasted 9 months, and the sensitivity of paclitaxel of HGC-27/PTX cells was significantly lower than parental cells (P＜0.05). Compared to parental cells, the morphology of HGC-27/PTX cells was slightly different, and the proportion of S and G2/M phase was obviously increased (P＜0.01). A total of 274 DEGs were identified between the resistant and parental cells with 130 genes up-regulated and 144 genes down-regulated. DEGs were significantly enriched in extracellular matrix (ECM)-receptor interaction (P＜0.001) and PI3K-Akt signaling pathways (P＜0.05), which could provide evidences for reversing paclitaxel resistance. Conclusions The paclitaxel-resistant gastric cancer cells HGC-27/PTX was established with stable culture in vitro, which provided an ideal model for future study on the mechanism of drug resistance.

Key words: Gastric cancer, Paclitaxel-resistance, RNAseq