Fig. 6: Inhibition of PI3Kδ activity improves canaliculus formation and differentiation in HepG2, Hep3B and HepaRG cells associated with the regulation of EMT and stemness markers. | Communications Biology

Fig. 6: Inhibition of PI3Kδ activity improves canaliculus formation and differentiation in HepG2, Hep3B and HepaRG cells associated with the regulation of EMT and stemness markers.

From: PI3Kδ activity controls plasticity and discriminates between EMT and stemness based on distinct TGFβ signaling

Fig. 6

a Immunoblot analysis of PI3Kδ protein level in Huh7, HepG2, Hep3B and HepaRG with the quantification of its relative intensity (right, n = 3 experiments). b RT-qPCR analysis of PI3Kδ expression in Huh7, HepG2, Hep3B and HepaRG cells; RPLP0 was used as the housekeeping gene for normalization. c Immunofluorescence staining for ZO-1 (green), actin microfilaments using phalloidin (red) and nuclei (blue) in HepG2, Hep3B and HepaRG cells plated in 3D cultures for 6 days and treated with the PI3Kδ specific inhibitor (CAL-101) at different doses. Scale bar: 10 µm d Quantification of the percentage of the different phenotypes seen in the conditions above (n = 40 organoids). e RT-qPCR analysis of several markers expression in HepG2, Hep3B and HepaRG cells plated in 3D culture and treated with different doses of CAL-101 for 6 days in two independent experiments performed in duplicate; RPLP0 was used as the housekeeping gene for normalization. All values are expressed as mean ± S.E.M.

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