Fig 2: The expression of miR-103 regulates the LATS2/YAP signaling pathway. (A) miR-103 regulates the protein level of LATS2, YAP, p-YAP (p-S127), CYR61, AREG, CTGF and CXCL5 (*P<0.05). (B) RT-qPCR analysis suggested that an increased miR-103 expression regulated the expression level of downstream of YAP target genes (*P<0.05). LATS2, large tumor suppressor kinase 2; YAP, yes-associated protein; CYR61, cysteine-rich angiogenic inducer; AREG, amphiregulin; CTGF, connective tissue growth factor; CXCL5, C-X-C motif chemokine 5.

Fig 3: LATS2 counteracts the effects of miR-103 on HCC cells. (A) Western blot analysis showing that LATS2 overexpression counteracts the promoting effects on the expression of EMT-related proteins induced by miR-103 (*P<0.05). (B) Transwell tumor cell invasion assay (magnification, ×200). (C) MTT cell proliferation assay (*P<0.05). HCC, hepatocellular carcinoma; NC, negative control; LATS2, large tumor suppressor kinase 2.

Fig 4: The prognostic significance of miR-103 and LATS2 combination in patients with HCC. (A) OS was compared between 4 subgroups of patients with HCC [miR-103 (high)/LATS2 (low), miR-103 (low)/LATS2 (low), miR-103(high)/LATS2 (high) and miR-103 (low)/LATS2 (high)] (**P<0.01). (B) DFS was compared between 4 subgroups of patients with HCC [miR-103 (high)/LATS2 (low), miR-103 (low)/LATS2 (low), miR-103 (high)/LATS2 (high) and miR-103 (low)/LATS2 (high)] (**P<0.01). HCC, hepatocellular carcinoma; LATS2, large tumor suppressor kinase 2; OS, overall survival; DFS, disease-free survival.