Objective:To investigate the antitumor lymphangiogenesis activity and mechanism of arsenic trioxide on transplantation tumor model for human breast infiltrating duct carcinoma in nude mice. Methods: The mice bearing tumor were randomly divided into 4 groups-negative control

positive control

experiment group 1 and 2

which were injected into a tail vein with sodium chloride

5-Fluorouracil(30 mg/kg) and arsenic trioxide (1.5 mg/kg or 3.0 mg/kg) for 7 days respectively. The intratumoral microlymphatics density (MLD) and expressions of vascular endothelial growth factor C(VEGF-C)

nuclear factor kappa-B P65

and Her2 protein were evaluated by immunohistochmistry methods. Reverse transcription-PCR was used to detect the expression of VEGF-C mRNA. Results: The tumors in arsenic trioxide groups showed significantly lower MLD than those in control groups(P<0.01)

and those in experimental group 2 were lower than those in experimental group 1(P<0.05).However

the expressions of VEGF-C in tumors of control groups were significantly higher than arsenic groups(P<0.01)

and those in experimental group 1 were higher than those in experimental group 2(P<0.05)

which were the same as VEGF-C mRNA in tendency. The expressions of P65 and Her2 in all groups were positively correlative with VEGF-C mRNA

with correlation coefficients of 0.782 and 0.848. Conclusion: Arsenic trioxide has obvious antitumor lymphangio genesis activity against transplantation tumor model for human breast infiltrating duct carcinoma in nude mice. Inhibiting the expression of P65 and Her2 and then down-regulating transcription of VEGF-C mRNA maybe its mechanism.