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. 2020 Mar 9;13:2127–2137. doi: 10.2147/OTT.S229913

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© 2020 Shi et al.

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miR-29b enhances sorafenib sensitivity by directly interacting with ATG9A in sorafenib-resistant HCC cells. (A) Predicted binding sites between miR‑29b and the ATG9A 3ʹ‑untranslated region by TargetScan online website. (B) Luciferase reporter assay shows miR-29b bind to wildtype ATG9A, not mutant ATG9A in 293T cells. (C) RT-qPCR shows the relative expression levels of ATG9A in HepG2 and Huh7 cells transfected with vector or ATG9A. (D, E) CCK-8 assay shows the effect of ATG9A overexpression on cell viability in HepG2 and Huh7 cells with ATG9A transfection and sorafenib treatment. (F) RT-qPCR shows the relative expression of HepG2/sora cells transfected with miR-NC, miR-29b, miR-29b+pcDNA, or miR-30b+ATG9A. (G) RT-qPCR shows the relative expression of Huh7/sora cells transfected with inh-miR-NC, inh-miR-29b, inh-miR-29b+siNC, or inh-miR-29b+si-ATG9A. (H, I) CCK-8 assay shows the cell viability of HepG2/sora and Huh7/sora cells in different transfected groups. (J, K) Western blotting shows the LC3-II/LC3-I protein ratio in HepG2/sora and Huh7/sora cells in different transfected groups. The data were presented as mean ± SD (*P < 0.05).