Fig. 8: ATXN3 promotes the progression of different subtypes of cervical cancer cells through P53 or p-STAT5.

A Effect of ATXN3 overexpression on P53 and p-STAT5 protein levels in C33A, HeLa, and SiHa cells. (n ≥ 3 independent cell cultures). B Statistical analysis of the effect of ATXN3 overexpression on p-STAT5 protein levels in C33A, HeLa, and SiHa cells. Each individual data point represents an independent cell culture experiment. C Statistical analysis of the effect of ATXN3 overexpression on P53 protein levels in C33A, HeLa, and SiHa cells. Each individual data point represents an independent cell culture experiment. D Effect of ATXN3 knockdown on P53 and p-STAT5 protein levels in C33A, HeLa, and SiHa cells. (n = 3 independent cell cultures). E Statistical analysis of the effect of ATXN3 knockdown on p-STAT5 protein levels in C33A, HeLa, and SiHa cells. Each individual data point represents an independent cell culture experiment. F Statistical analysis of the effect of ATXN3 knockdown on P53 protein levels in C33A, HeLa, and SiHa cells. Each individual data point represents an independent cell culture experiment. G Changes in ATXN3, P53, and p-STAT5 protein levels in C33A, HeLa, and SiHa cells after ATXN3 overexpression or knockdown under hypoxic conditions. (n = 3 independent cell cultures). H Statistical analysis of changes in ATXN3, P53, and p-STAT5 protein levels in C33A, HeLa, and SiHa cells after ATXN3 overexpression or knockdown under hypoxic conditions. Each individual data point represents an independent cell culture experiment. The statistical notations used in the figure are:ns P > 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001. Data are represented as mean ± SD. Two-tailed unpaired Student’s t -test was employed for analyses in panels (B, C, E and F), while One-way ANOVA were performed for panels (H).