Research Paper Volume 13, Issue 10 pp 13405—13420

Inhibition of CXCR2 plays a pivotal role in re-sensitizing ovarian cancer to cisplatin treatment

Generation of a pan-resistant ovarian cancer (OC) cells (ACRP) from its parental sensitive counterpart (A2780). (A) ACRP is 3.64-fold more resistant to cisplatin (1.5uM - 100uM) than A2780. (B) ACRP is 77.27-fold more resistant to paclitaxel (1 nM - 10 μM) than A2780. (C) ACRP is 21.42-fold more resistant to doxorubicin (0.1uM - 100uM) than A2780. Estimated IC50 for drugs in tested lineages were calculated by MTT assay, following 24h of cells treatment with each drug within the aforementioned concentration ranges of drugs, which correlate to their circulating concentration in EOC patients. Results are expressed as percentage of control (untreated cells) as mean ± SD. Statistical analyses of the results were done by two-way ANOVA followed by Bonferroni post- test. *pp

Figure 1. Generation of a pan-resistant ovarian cancer (OC) cells (ACRP) from its parental sensitive counterpart (A2780). (A) ACRP is 3.64-fold more resistant to cisplatin (1.5uM - 100uM) than A2780. (B) ACRP is 77.27-fold more resistant to paclitaxel (1 nM - 10 μM) than A2780. (C) ACRP is 21.42-fold more resistant to doxorubicin (0.1uM - 100uM) than A2780. Estimated IC50 for drugs in tested lineages were calculated by MTT assay, following 24h of cells treatment with each drug within the aforementioned concentration ranges of drugs, which correlate to their circulating concentration in EOC patients. Results are expressed as percentage of control (untreated cells) as mean ± SD. Statistical analyses of the results were done by two-way ANOVA followed by Bonferroni post- test. *p<0.01, **p<0.005, ***p<0.001. N=3.