Abstract: Objective To explore the effect of TNF-α on expression of TROP-2 and to explore the role of TROP-2 in the metastasis and invasion of colon cancer HCT-116 cells. Methods HCT-116 cells were cultured and treated with 0, 10, 20, 30, 50, 100 and 200 μg/L TNF-α. Cell viability was assessed by MTT. The expression of TROP-2 was determined by western blot. The effects of 20 μg/L TNF-α on cell migration and invasion were investigated by wound healing assay and Transwell method. Small interfering RNA (siRNA) was used to knock down endogenous TROP-2 expression. The transcrip⁃ tion and translation levels of TROP-2 were detected by qPCR and Western blot respectively. The migratory and invasive ca⁃ pability of HCT-116 cells transfected with TROP-2 siRNA were checked by wound healing assay and Transwell method re⁃ spectively. Results There is no significant change of cell viability between HCT-116 cells treated with 0,10, 20, 30 and 50 μg/L TNF-α, but cell viability of HCT-116 decreased significantly with treatment of 100 μg/L and 200 μg/L TNF-α. Low concentration of TNF-α (≤50 μg/L) led to increase of TROP-2 protein expression that peaks when 20 μg/L TNF-α was add⁃ ed. High concentration of TNF-α (100, 200 μg/L) result in decrease of TROP-2 protein. TROP-2 siRNA significantly downregulated the expression of TROP-2 at both mRNA and protein levels in colon cancer HCT-116 cells. Compared with con⁃ trol group, silencing TROP-2 by TROP-2 siRNA inhibited the migratory and invasive capability of HCT-116 cells. Wound healing rate and the number of transwell cell both decreased in siRNA group compared with those of control group (P < 0.05). Conclusion The mechanism that low concentration of TNF-α promoted HCT-116 cells migration and invasion might be through up-regulating the expression of TROP-2.

Key words: colonic neoplasms, tumor necrosis factor-alpha, neoplasm invasiveness, cell movement, TROP-2