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. 2018 May 11;9(5):562. doi: 10.1038/s41419-018-0631-9

Fig. 3. UHRF1 was overexpressed in the docetaxel-resistant cancer cells, which contributed to the maintenance of the CSC phenotype.

Fig. 3

a The protein levels of UHRF1 were analyzed in CNE2 and CNE2TR cells, DU145 and DU145-DR cells, and SKOV3 and SKOV3R cells by Western blot. b The depletion of UHRF1 in DU145-DR and CNE2TR cells decreased the CSC sub-population. DU145-DR and CNE2TR cells were infected with lentivirus-delivered shRNA-UHRF1 or shRNA-CTR. Cells were labeled with fluorescent antibodies against CD44 (APC) and CD133 (PE). CD44highCD133high cells were detected by flow cytometry. c CNE2TR and DU145-DR cells were infected with lentivirus-delivered shRNA-UHRF1 or shRNA-CTR. One thousand cells were re-seeded in culture media-mixed agarose, and the cell spheres formed were stained with crystal violet and analyzed 21 days after cell seeding. The spheres were counted in five randomly selected fields, and the difference of spheres in two groups was compared by statistical analysis. d UHRF1 depletion decreased the expression of CSC-associated molecules ALDH1, NANOG, SOX2, and SHH in CNE2TR and DU145-DR cells. e UHRF1 overexpression elevated the levels of CSC-associated molecules ALDH1, NANOG, SOX2 and SHH in CNE2, and DU145 cells