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Fig. 2 | Journal of Hematology & Oncology

Fig. 2

From: Therapeutic strategies of drug repositioning targeting autophagy to induce cancer cell death: from pathophysiology to treatment

Fig. 2

Nuclear translocation of MiT/TFE protein is responsible for the constitutive activation of autophagy–lysosome pathway in cancer cells. Compared with normal cells, greater amounts of MiT/TFE transcriptional factors (i.e., MITF, TFE3, and TFEB) accumulate in the nuclei of cancer cells under nutrient-insufficient conditions. These transcriptional factors drive expression of genes related to autophagylysosome flux. Surprisingly, even under mTOR-inactivated conditions (such as starvation), cancer cells express high levels of Mit/TFE proteins in the nucleus, which may explain the constitutive activation of autophagy independent of mTOR signaling. Note that the red bar indicates the enhanced autophagic activation, while the blue bar indicates the suppressed autophagic regulation

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