Research Paper Volume 11, Issue 2 pp 350—370

BCL2L10/BECN1 modulates hepatoma cells autophagy by regulating PI3K/AKT signaling pathway

Figure 6. Overexpression of BCL2L10 inhibited autophagy of Hep3B cells by binding to BECN1. (A) The expression of BCL2L10 and BECN1 after transfection in four different groups was detected by qRT-PCR. (B) The cell viability of pcDNA3.1-BECN1 group was the weakest, while the cell viability of pcDNA3.1-BCL2L10 group was the strongest. (C) Overexpression of BECN1 facilitated the accumulation of LC3B puncta in Hep3B cells as detected by immunofluorescence. (D) The expression of LC3B-II/LC3B-I in pcDNA3.1-BCL2L10 group was decreased while the expression of LC3B-II/LC3B-I in pcDNA3.1-BECN1 group was increased. The changes of P62 had a contrary trend with changes of LC3B-II/LC3B-I. (E) Degradation of P62 was little observed in the presence of Bafilomycin A1 (an inhibitor of late-phase autophagy), while LC3B-II/LC3B-I expression was increased in Hep3B cells. * P <0.05.