Fig. 7

ALKBH5 enhanced BCL-2 mRNA stability by catalyzing m6A demethylation and promoted the interaction between Bcl-2 and Beclin1. a Gene-specific m6A qPCR analysis of m6A level in mRNA transcripts of ALKBH5 in SKOV3 cells infected with LVRU6P-01, LVRU6P-02, or LVRU6P-NC. b Gene-specific m6A qPCR analysis of m6A level in mRNA transcripts of ALKBH5 in A2780 cells infected with LV121-NC or LV121-ALKBH5. c SKOV3 cells infected with LVRU6P-01, LVRU6P-02, or LVRU6P-NC. d A2780 cells were infected with LV121-NC or LV121-ALKBH5, followed by treatment with vehicle or flavopiridol for 6 h. The mRNA levels of BCL-2 were measured by RT-qPCR, and the F/V ratio of NANOG mRNA was determined. e Relative luciferase activity of pMIR-REPORT-BCL-2-3′-UTR with either wild-type or mutant (A-to-T mutation) m6A sites after co-transfection with LV121-ALKBH5 or LV121-NC into A2780 cells. Firefly luciferase activity was measured and normalized to Renilla luciferase activity. f Luciferase assays were performed in A2780 cells transfected with wild-type or mutant luciferase-BCL-2-3′-UTR reporter. g SKOV3 cells were infected with LVRU6P-01, LVRU6P-02, or LVRU6P-NC. A2780 cells were infected with LV121-NC or LV121-ALKBH5. Then, the expression of Bcl-2 and Beclin1 was determined by WB. h SKOV3 cells were infected with LVRU6P-01, LVRU6P-02 m or LVRU6P-NC. A2780 cells were infected with LV121-NC or LV121-ALKBH5. Subsequently, the immunoprecipitation of endogenous Beclin1 with endogenous Bcl-2 was performed. Error bars represent the standard error. * indicated P < 0.05