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. 2021 Aug 31;29(2):381–392. doi: 10.1038/s41418-021-00862-4

Fig. 7. FBXW2-p65 axis is involved in regulating breast cancer cell paclitaxel resistance.

Fig. 7

A Total cell lysates from MCF-7 and MCF-7/TaxR cells were prepared. Immunoblotting analyses were performed. B MCF-7 and MCF-7/TaxR cells were prepared. Immunofluorescence was performed. C p65 was knocked down in MCF-7/TaxR cells. Cell proliferation rates were measured by cell counting. D FBXW2 was stably overexpressed in MCF-7/TaxR cells. Cell proliferation rates were measured by cell counting. E MCF-7/TaxR cells with stable expression of FBXW2 were treated with 10 nM paclitaxel for two days. Cell proliferation rates were measured by cell counting. F-H MCF-7/TaxR cells were injected into nude mice. After 7 days, the mice were randomly assigned to four groups: PBS (control), paclitaxel, HA-FBXW2 overexpression and HA-FBXW2 overexpression combined with paclitaxel, and given intraperitoneally three times each week for treatment. After 14 days of treatment, the mice were sacrificed, and the tumor weight was measured. Tumor volume was measured during the tumor growth for 3 weeks. (All data represent mean ± SEM n ≥ 3), *p < 0.05.