Fig. 5

Exploration of mRNA m¹A modification was associated with autophagy in hepatocellular carcinoma (HCC) cells. (A) Expression of LC3I, LC3II, Beclin 1, and p62 in Earle’s balanced salt solution (EBSS)–treated HepG2 or QGY cells for 6, 12 h and their corresponding control cells assessed using western blot (left) and quantitatively analyzed (right); (B) Cell proliferation assays to detect the effects of EBSS on HCC cells; (C) Levels of mRNA m¹A modification in EBSS-treated HepG2 cells for 0, 6, 12, 18, 24, and 30 h assessed through dot blot assay. Expression of LC3I and LC3II in the above groups assessed through western blotting and quantitatively analyzed (right); (D) Expression of LC3I, LC3II, Beclin 1, and p62 in sh-ALKBH3 HepG2 cells and their corresponding control cells assessed through western blot (up) and quantitatively analyzed (down); (E) shNC and shALKBH3 HepG2 cells were transfected with vector control, ALKBH3, ALKBH3-R122S, or ALKBH3-L177A constructs for 48 h, the expression of LC3I, LC3II, Beclin 1, and p62 were checked (up) and quantitatively analyzed (down); (F and G) Relative fold of the proliferation (F) and colonization (G) of HepG2 cells treated with EBSS and the ALKBH3 overexpression group and the control group. Data are presented as mean ± standard deviation from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 compared with the control group