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Fig. 3 | Journal of Translational Medicine

Fig. 3

From: Periostin involved in the activated hepatic stellate cells-induced progression of residual hepatocellular carcinoma after sublethal heat treatment: its role and potential for therapeutic inhibition

Fig. 3

POSTN induced the Shc-ERK activation of heat-exposed residual HCC cells through integrin β1. a The mRNA expression profile of heat-treated residual MHCC97H cells in response to POSTN was illustrated as a heatmap. Red, green represent high and low mRNA expression. b With POSTN treatment, the phosphorylated of p52Shc and ERK1/2 in heat-exposed residual HCC cells (MCHCC97H and HepG2) were significantly increased in a time-dependent manner. c PPI network analysis of the differentially expressed genes identified Shc as a gene of biological importance in POSTN-mediated signaling networks and a diagram illustrated the interaction of Shc with the molecules (e.g., ITGB1 and MAPK1). d When heat-exposed residual HCC cells (MCHCC97H and HepG2) were treated with POSTN, the levels of PCNA, N-cadherin and ERK1/2 phosphorylation were significantly increased. ERK1/2 inhibitor (U0126, 25 μM) reversed the above POSTN-induced increase. e With the stimulation of exogenous POSTN, the levels of Ki-67, PCNA and Snail mRNA expression were significantly decreased in heat-exposed residual integrin β1-knockdown MHCC97H cells. f Expression of POSTN in HCC tissues (n = 374) than that of adjacent non-tumor tissues (n = 50) in the HCC data of TCGA cohorts. g A significant positive correlation between the degree of POSTN expression also showed with that of COL1A1 (r = 0.8445, P < 0.0001), Ki-67 (r = 0.1928, P = 2×10−4), Snail (r = 0.6395, P < 0.0001), and Sch3 (r = 0.1121, P = 0.0304) in the TCGA-HCC cohorts. h HCC patients were stratified by POSTN and MAPK1 (ERK2) expression and the co-expression of POSTN and ERK2 predicted poor-survival prognosis in the TCGA-HCC cohorts by Kaplan–Meier analyses

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