Fig. 7

TGFβRII served as a direct target of miR-6766-3p. a The efficiency of transfection with miR-6766-3p mimic in LX2 cells was verified by qPCR. b, c The expression changes of TGFβRII and fibrosis-related genes (α-SMA, COLLAGEN I, TIMP1, TIMP3, MMP2, and MMP9) regulated by miR-6766-3p were verified by qPCR in LX2 cells and activated LX2 cells treated with miR-6766-3p mimic and its NC. d TGFβ induced profibrogenic protein expressions in activated LX2 cells, such as COLLAGEN I, α-SMA and KI67, whereas they were inhibited by miR-6766-3p after treatment with miR-6766-3p mimic or its NC. e Quantification of integrated optical density of genes in d. f Cell proliferation was measured using cell viability assay with CCK8 kit in LX2 cells and TGFβ-induced LX2 treated with miR-6766-3p mimic and its NC. g Flow cytometry assay was performed to determine the changes of calcium content in LX2 cells and activated LX2 cells after the addition of the miR-6766-3p mimic and its NC. h Quantification of cell cycle with the forced expression of miR-6766-3p measured by flow cytometry in LX2 cells and activated LX2 cells after treatment with the miR-6766-3p mimic and its NC. (Flow cytometry analysis used to determine the stages of cell cycle was provided in Additional file 1.). i Quantification of wound recovery rates modeled by cell scratch assays, in LX2 cells and activated LX2 with different treatments, and the migration index was presented over time. (The images of cell scratch assays were provided in Additional file 1.). Data represent the mean ± SEM. *P < 0.05, **P < 0.01, and ***P < 0.001