The enhancement of autophagy flux by TGFβ depends on the protein levels of MAP1S.

<p>A,B) Immunoblotting analyses (A) and plots (B) of the impact of TGFβ on autophagy flux marker LC3-II in MEF cells developed from wild-type (MAP1S+/+) or MAP1S knockout mice (MAP1S-/-) in the absence (Ctrl) or presence of Bafilomycin A1 (BAF). C,D) Immunoblotting analyses (C) and plots (D) of the impact of TGFβ on autophagy flux marker LC3-II in MEF cells developed from wild type mice (MAP1S+/+) treated with mixture of random sequence siRNAs (MOCK) or MAP1S-specific siRNA (MAP1S) in the absence or presence of BAF. E,F) Immunoblotting analyses (E) and plots (F) of the impact of TGFβ on autophagy flux marker LC3-II in MEF cells developed from knockout mice (MAP1S-/-) transiently transfected with empty vector (HA) or plasmid carrying HA-MAP1S in the absence or presence of BAF. G,H) Immunoblotting analyses (G) and plots (H) of the impact of TGFβ on autophagy flux marker LC3-II in Capan-2 cells treated with mixture of random sequence siRNAs (MOCK) or MAP1S-specific siRNA (MAP1S) in the absence or presence of BAF. The same amounts of total proteins were loaded and β-Actin served as another control. The relative intensities of LC3-II in untreated wild type cells were set as 1. Data were the means ± S.D. of at least three repeats and the significance of differences was tested by Student’s t test. *, P≤0.05; **, P≤0.01; and unlabeled, not significant. I) A diagram showing the mechanism by which TGFβ suppresses tumorigenesis through MAP1S-mediated autophagy flux.