Fig. 2

CCL2 correlates with TAMs accumulation and tissue inflammation in nitrosamine-induced esophageal carcinogenesis. a NMBA induces notable tumors in ESCC rat model. b Expression of CCL2 in rat esophageal epithelium is increased at mRNA and protein levels during carcinogenesis (n = 5). c Representative IHC staining indicates the expression of CCL2 and CD68 during rat esophageal carcinogenesis resembling human ESCC. d Expression of CCL2 increases with pathologic progression in rat model (n = 9). e Accumulation of CD68⁺ TAMs is correlated with CCL2 expression. f Increased expression of inflammatory cytokines during esophageal carcinogenesis (n = 5). g The basal levels of CCL2 between normal human esophageal epithelium cells (Het-1A) and the ESCC cells (TE-1). h NMBA treatment continuously increases CCL2 expression over time. i Chemotaxis of THP-1monocyte is increased by conditioned medium from the transformed cells and TE-1 cells. j Monocyte chemotaxis induced by transformed cells is antagonized by CCL2-neutralizing antibody in a dose-dependent manner. Data is shown by mean ± standard deviation from three independent experiments. When compared to the control group, * indicates P < 0.05, ** indicates P < 0.01