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Fig. 8 | Journal of Experimental & Clinical Cancer Research

Fig. 8

From: Chlorpromazine induces cytotoxic autophagy in glioblastoma cells via endoplasmic reticulum stress and unfolded protein response

Fig. 8

Mechanisms that can explain CPZ toxicity towards GBM cells while partially sparing RPE-1 non-cancer cells. CPZ exerts a role in affecting GBM cell growth and survival. CPZ ignites in GBM, via ER stress, UPR and ROS generation, a non-apoptotic cell death, mainly related to cytotoxic autophagy and induction of nuclear aberrations that culminate in a mitotic catastrophe (left). Our data highlight the higher toxicity of the drug towards GBM cells than RPE-1 non-cancer cells, possibly due to the ability of the latter to conduct a more proficient, survival-oriented, autophagic process (right)

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