FIGURE 6.

VAMP2 abated the functions of miR‐383‐5p on HCC progression and chemosensitivity of Oxa. (A,B) Transfection efficiency of si‐VAMP2 in Hep3B cells and transfection efficiency of oe‐VAMP2 in Huh7 cells were determined by qRT‐PCR and western blot assays (t‐test). (C–G) Hep3B cells were transfected with inhibitor NC, miR‐383‐5p inhibitor, miR‐383‐5p inhibitor + si‐NC, or miR‐383‐5p inhibitor + si‐VAMP2 and Huh7 cells were transfected with mimic NC, miR‐383‐5p mimic, miR‐383‐5p mimic + Vector, or miR‐383‐5p mimic + oe‐VAMP2, and then these cells were treated with different concentrations of Oxa (C,D) or 6 μM Oxa (E–G). (C,D) CCK‐8 assay was utilized to assess the cell viability and IC50 of Oxa value (ANOVA). (E) Colony formation ability was evaluated using a colony formation assay (ANOVA). (F) Cell apoptosis was analyzed using flow cytometry analysis (ANOVA). (G) Western blot assay was carried out to measure the protein levels of cyclinD1 cleaved‐caspase‐3, LC3I/II, and p62 (ANOVA). *p < .05. ANOVA, analysis of variance; CCK‐8, Cell Counting Kit‐8; HCC, hepatocellular carcinoma; LC3, light Chain 3; NC, negative control; qRT‐PCR, quantitative real‐time polymerase chain reaction; VAMP2, vesicle‐associated membrane protein‐2