Bladder cancer is the tenth most common cancer in the world. hAM homogenate is a promising approach to treat it. We used different methods (qPCR, Western blotting and immunolabelling) to investigate how hAM homogenate affects the expression of selected genes, as well as the expression and presence of selected proteins related to autophagy, in normal and cancer urothelial cells. The results indicate that hAM homogenate slightly decreased the expression of some genes (GOLPH3, BECN1, MAP1LC3B and SIRT1) in normal and cancer urothelial cells. We showed a statistical difference only in the expression of GOLPH3 in cancer urothelial cells. Furthermore, the results show that hAM homogenate slightly decreased the expression of proteins GOLPH3 and Beclin1 and increased the expression of LC3B II protein in cancer cells, but not statistically significant. Immunofluorescence confirmed the results of Western blotting results for GOLPH3 and Beclin1, but not for LC3B, with immunofluorescence showing lower expression of LC3B in treated cancer cells. We also found that hAM homogenate either increases the redistribution of GOLPH3 to the Golgi apparatus in cancer urothelial cells or influences GOLPH3 to remain present in the Golgi apparatus. Whereas in normal urothelial cells it triggers redistribution to the larger part of the cytoplasm. Based on the results, we conclude that hAM homogenate can inhibits autophagy in cancer urothelial cells by different mechanisms, but not in normal urothelial cells. We believe that the effect of hAM homogenate on autophagy represents a potential area for further research related to the treatment of bladder cancer.
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